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1
Renaux, Sophie. "Eimeria du lapin : étude de la migration extra-intestinale du sporozoïte et du développement de l'immunité protectrice." Tours, 2001. http://www.theses.fr/2001TOUR3802.
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Moulia, Catherine. "Modalités des interactions génétiques dans les systèmes hôte-parasite : l'association nématodes (oxyures) : muridés (Mus) en zone d'hybridation hôte." Montpellier 2, 1992. http://www.theses.fr/1992MON20199.
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La dysgenese d'individus au genome recombinant du centre de la zone hybride entre les deux sous-especes de souris domestiques europeennes mus musculus domesticus et m. M. Musculus est etudiee a travers les modalites de resistance/susceptibilite des souris aux nematodes intestinaux (oxyures). Nous verifions et confirmons tout d'abord in situ dans la partie danoise de la zone d'hybridation hote la surinfestation hybride constatee en allemagne par d'autres auteurs; puis, nous montrons par des infestations experimentales controlees de souris de type parental et de souris de la zone hybride danoise, le determinisme genetique du phenotype parasitaire (charge) de resistance/susceptibilite vis-a-vis d'un nematode intestinal (oxyure); nous avons realise des croisements experimentaux de souris de type parental resistantes aux oxyures (f1, f2 et retrocroisements). Les resultats d'infestations de ces souris montrent l'apparition de la susceptibilite en f2 et back-cross. Ceci confirmerait l'hypothese selon laquelle les associations alleliques generees par la recombinaison des deux genomes seraient peu fonctionnelles. Enfin, pour acquerir des informations sur le determinisme genetique de la resistance/susceptibilite des souris aux oxyures nous avons analyse le phenotype parasitaire de lignees consanguines. Des hybrides f1 issus d'une lignee sensible et de lignees resistantes presentent une sensibilite intermediaire suggerant l'existence d'une codominance. Les resultats sont discutes au niveau individuel (mecanismes immunogenetiques) et populationnel (parasitisme en zone hybride hote)
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Cellier, Mathieu. "Elaboration de modèles expérimentaux pour l'étude des stress cellulaires dans les interactions hôte - agent pathogène." Montpellier 2, 1992. http://www.theses.fr/1992MON20205.
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Au cours de processus infectieux, les interactions entre pathogenes intracellulaires et macrophages peuvent declencher des reactions cellulaires apparentees a la reponse au choc thermique. Ces reactions impliquant des proteines specifiques appelees proteines de stress (hsp) ont ete etudiees en utilisant comme modele la lignee leucemique humaine u937 et la bacterie brucella. Nous avons montre qu'un choc thermique sub-lethal permet d'induire la differenciation des cellules myelomonocytaires. Les resultats obtenus suggerent une adaptation fonctionnelle au stress des cellules monocytaires permettant d'accelerer leur maturation en macrophages lors d'etats febriles. Les hsp majeure dnak (hsp70) et dnaj (hsp40), groe1 (hsp60) et groes (hsp10) de brucella ovis ont ete clonees. L'operon dnak-j a ete sequence; il est exprime dans e. Coli et permet de complementer un mutant deficient en dnak. La dnak de brucella ovis est d'autre part apparue comme un antigene majeur au cours de l'infection. La caracterisation moleculaire d'un fragment de hsp60 a permis de preciser la taxonomie du genre brucella. La conservation structurale des hsp70 au cours de l'evolution a permis d'analyser l'origine phylogenetique de brucella ovis
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Nicolas-Gaulard, Isabelle. "Activité immunomodulatrice d'une protéine, l'hypodermine A, sur les cellules sanguines mononucléées des bovins." Paris 12, 1995. http://www.theses.fr/1995PA120031.
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Parmi les grandes maladies parasitaires qui affectent le cheptel bovin francais, l'hypodermose est responsable de pertes economiques importantes. Le premier stade larvaire de l'insecte responsable de cette parasitose provoque une desorganisation des systemes de defense de l'hote. Ces defaillances sont causees par les secretions larvaires et principalement par l'hypodermine a (ha). L'objet de ces travaux est l'etude de l'activite immunomodulatrice de l'ha sur les cellules sanguines mononucleees des bovins. L'ha inhibe la proliferation des lymphocytes apres stimulation par une lectine mitogene ou par un agent chimique et agit sur la phase precoce de l'activation cellulaire. De plus, l'indometacine, qui inhibe la synthese des prostaglandines, restaure la reponse proliferative des pbmc. La production en pge#2 est augmentee par l'ha dans les cultures de pbmc ou de monocytes. Les concentrations en pge#2 equivalentes a celles dosees dans les cultures en presence d'ha sont inhibitrices de la reponse proliferative a la phytohaemagglutinine. L'ha agirait donc sur la diminution de la reponse des pbmc par une voie dependante des prostaglandines. L'ha induit une baisse de la production d'il2 et beaucoup moins importante de l'ifn dans ces cultures stimulees par la phytohaemagglutinine. Une restauration de la proliferation des lymphocytes est observee par adjonction de surnageant enrichi en il2. La fonction accessoire des monocytes et la production de no, qui sont impliquees dans la proliferation des lymphocytes, sont inhibees par l'ha. L'ha module egalement l'expression de differents marqueurs a leur surface. Tous ces mecanismes decrits in vitro pourraient expliquer les phenomenes d'echappement du parasite au systeme immunitaire du bovin
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Gay, Frédérick. ""Chimiorésistance de "Plasmodium falciparum" : études sur les populations impaludées et sur les populations plasmodiales"." Montpellier 2, 1992. http://www.theses.fr/1992MON20277.
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La chimioresistance de plasmodium falciparum est etudiee a travers les populations impaludees et au sein des populations plasmodiales. Les trois outils mis en uvre sont l'epidemiologie, la recherche clinique et la recherche fondamentale. Les resultats concernant les populations impaludees portent sur l'evolution des taux d'incidence d'acces palustre chez les voyageurs, l'evolution des taux de prevalence et des niveaux de chimioresistance en afrique de l'ouest et le role de la biodisponibilite dans l'interpretation des echecs therapeutiques. Les travaux portant sur les populations plasmodiales contribuent a l'etude des clones parasitaires, revelent une resistance croisee entre les aryls-amino-alcools et reproduisent experimentalement les effets de la pression medicamenteuse in vitro. Nous poursuivons nos recherches avec le meme objectif qu'est de degager des alternatives therapeutiques au vu de donnees fondamentales, cliniques et epidemiologiques dans l'espoir de contribuer a la lutte antipaludique
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Dupas, Stéphane. "La suppression immunitaire dans le système drosophile-parasitoi͏̈de : aspects physiologiques, génétiques et évolutifs." Montpellier 2, 1998. http://www.theses.fr/1998MON20015.
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L'objectif de cette these est d'etudier les variations de l'aptitude immunosuppressive du parasitoide leptopilina boulardi vis-a-vis de son l'hote drosophila melanogaster d'un point de vue physiologique, genetique et evolutif. D'un point de vue physiologique nous avons montre que la reaction de l'hote se mettait en place suite au depot precoce d'une fine couche dense aux electrons a la surface du chorion de l'uf (vraisemblablement de la melanine). De son cote, le parasitoide produit des particules d'allure virale (vlps) responsables de l'immunosuppression et reagissant positivement aux colorations de l'adn. Une variation morphologique des particules de l. Boulardi s'est averee etre correlee a la variation de l'aptitude immunosuppressive. D'un point de vue genetique nous avons pu montrer par des croisements entre souches d'aptitude immunosuppressive opposee que les vlps etaient transmis genetiquement sous une forme integree aux chromosomes. Plusieurs genes d'immunosuppression, chacun specifique d'une espece hote, ont ete mis en evidence. D'un point de vue evolutif, une adaptation locale des genes de suppression immunitaire au spectre d'hote present dans la localite est clairement observee. Enfin, des systemes genetiques de resistance a l'immunosuppression sont suggeres par nos resultats, ceux-ci pourraient etre a l'origine d'une certaine complementarite observee entre les genes de l'hote et du parasitoide. Mots cles : immunosuppression, vlps, coevolution hote-parasitoide, genetique des interactions.
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Laugier, Claire. "Contribution à l'étude des infestations par des petits strongles chez le cheval en Normandie : données épidemiologiques et aspects lésionnels." Montpellier 2, 2002. http://www.theses.fr/2002MON20125.
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Girod, Anne. "Production de vecteurs rétroviraux par des lignées transcomplémentantes aviaires : augmentation du titre en vecteurs et analyse des formes virales parasites produites." Lyon 1, 1995. http://www.theses.fr/1995LYO10312.
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Le laboratoire a developpe, a partir de retrovirus aviaires de type alsv, des lignees transcomplementantes productrices de particules vecteurs en condition helper-free. Nous avons ici recherche a augmenter le titre en particules produites par ces lignees transcomplementantes et analyse les formes virales recombinantes generees par ces systemes. L'introduction du genome vecteur dans la lignee d'empaquetage par infection plutot que par transfection a permis d'accroitre les titres des stocks de vecteurs retroviraux a des valeurs de 10#6 efu-(expressing forming unit)/ml. En revanche, le systeme ping-pong decrit pour les vecteurs retroviraux murins n'a pas permis d'obtenir l'amplification escomptee des titres en virus vecteurs. En outre, dans de telles cocultures, il apparait un virus competent pour la replication, qui porte les fonctions trans des genomes transcomplementants et les fonctions cis du genome vecteur. Les genomes transcomplementants sont deletes de la sequence d'encapsidation et de sequences necessaires a la transcription inverse et l'integration. Cependant, des arn transcrits a partir de ces genomes peuvent etre encapsides, retrotranscrits et s'integrer dans l'adn de la cellule cible. Ce transfert parasite, de l'ordre de 1 particule pour 10#5 particules vecteurs, peut etre explique par des evenements de recombinaison retrovirale entre le genome transcomplementant et le genome vecteur coencapsides. Ces formes virales parasites defectives pour la replication pourraient conduire, apres plusieurs cycles de replication successifs, a l'emergence de formes virales completes, comme celles observees dans le surnageant des cocultures decrites ci-dessus. Le genome des cellules de poule contient des sequences dites endogenes dont la structure est proche de celle des retrovirus. Lorsque les cellules lmh de leghorn noire sont utilisees pour la construction de lignees transcomplementantes, la presence de l'endogene ev3 conduit a la generation de formes virales parasites defectives pour la replication. Celles-ci representent 1% des particules virales produites. Ces resultats permettent d'obtenir une meilleure connaissance des systemes de production de vecteurs retroviraux
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BAHRI, SIHEM, and ADAM MARQUES. "Etude comparee de quelques myxosporidies parasites de poissons mugilidae de mediterranee occidentale : aspects structuraux, biologiques et immunologiques." Montpellier 2, 1997. http://www.theses.fr/1997MON20005.
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Cette etude porte sur les myxosporidies parasites des muges de mediterranee occidentale principalement mugil cephalus et liza ramada provenant du lac ichkeul de tunisie. Les donnees ultrastructurales ont permis de differencier 7 especes du genre myxobolus dont trois nouvelles m. Bizerti n. Sp. ; m. Ichkeulensis n. Sp. ; m. Ramadae n. Sp. , formant des kystes branchiaux. Trois formes viscerales ont ete identifiees: m. Spinacurvatura ; m. Mulleri, localisees dans les vaisseaux mesenteriques et m. Exiguus infestant la paroi intestinale. La 7eme espece recoltee au niveau du tegument a ete rattachee a m. Espisquamalis, responsable du rejet commercial des poissons atteints. Les caracteres ultrastructuraux des kystes et des stages sporogoniques ont ete decrits. Leur action pathologique a ete examinee. L'incidence sur l'embonpoint de leurs hotes ainsi que le facteur de risque d'infestation de ces parasites lie a la taille de l'hote ont ete analyses. L'obtention d'une sonde anticorps polyclonale anti-myxobolus episquamalis, a permis de realiser une etude antigenique de ce parasite, de determiner des antigenes specifiques, d'autres communs a plusieurs especes de myxosporidies etudiees et de demontrer une parente antigenique entre myxobolus episquamalis et son hote mugil cephalus
10
Ben, Abderrazak Souha. "Variabilité génétique des populations de "Plasmodium falciparum"." Montpellier 2, 1993. http://www.theses.fr/1993MON20013.
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Nous avons analyse par electrophorese d'isoenzymes (7 a 12 loci) le polymorphisme genetique de 5 populations (113 stocks) du plasmodium falciparum, l'agent de la forme la plus severe de paludisme. Les resultats ont ete interpretes en termes de genetique des populations, dans le but d'analyser la structure des populations naturelles de ce parasite. Un fort desequilibre de liaison apparait dans trois des populations etudiees, ainsi que dans l'echantillon global. Une quatrieme population montre egalement des indices de desequilibre, quoique dans une moindre mesure. Une seule serie n'a montre aucune deviation par rapport aux predictions de la panmixie. Ces resultats ne sont explicables, ni par la structuration geographique des populations, ni par la selection naturelle. L'hypothese la plus parcimonieuse pour rendre compte de nos donnees est l'existence d'une propagation uniparentale chez p. Falciparum dans certaines circonstances. De forts indices d'autofecondation peuvent expliquer ce resultat. La structure des populations naturelles de plasmodium falciparum et le mode de reproduction du parasite ont des consequences importantes sur l'epidemiologie de la maladie. Le modele subclonal ou partiellement clonal que nous proposons ici est radicalement different, quant a ses implications taxonomiques et epidemiologiques, du modele potentiellement panmictique qui avait ete propose pour p. Falciparum. En effet, si des lignees parasitaires subissent une propagation uniparentale, elles se comportent comme des clones, et gardent intactes leurs caracteristiques genetiques d'une generation a l'autre, tandis que le patrimoine genetique de chaque genotype fait l'objet d'un brassage energique a chaque generation dans le cas du modele potentiellement panmictique. Les problemes poses sont: (a) la nature du processus de reproduction uniparentale; (b) l'importance respective des cycles sexues et asexues; (c) la stabilite dans l'espace et dans le temps des lignees uniparentales
11
Bekkaoui, Abdelhamid. "Rôle de stimulus chimiques de contact dans la reconnaissance des chrysalides-hôtes par diadromus pulchellus Wsm. (hymenoptera), parasitoïde du phytophage acrolepiopsis assectella Zell. (lepidoptera)." Tours, 1992. http://www.theses.fr/1992TOUR4005.
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Le comportement de reconnaissance de l'hôte par l'hyménoptère diadromus pulchellus wsm, parasitoïde des chrysalides d'acrolepiopsis assectella zell, la teigne du poireau, semble détermine en très grande partie, sinon exclusivement, par des stimulus chimiques de contact liés à la cuticule et au cocon de l'hôte. Ces kairomones semblent être des molécules hydrophiles de faible taille et très spécifiques. Elles ne sont en effet pas retrouvées dans la soie de lépidoptères non hôtes. L'élevage de la teigne sur un milieu artificiel pauvre en substances du poireau ou même n'en contenant pas du tout, à la place du poireau, ne semble aucunement affecter les réponses comportementales des femelles de d. Pulchellus vis-à-vis des kairomones de l'hôte. Ces kairomones sont donc d'origine endogène et ne dérivent pas de composés du poireau. La comparaison de d. Pulchellus à une espèce proche, diadromus collaris grav. Attaquant aussi a. Assectella montre une faible adaptation de la seconde espèce vis-à-vis de cet hôte. Un apprentissage associatif de courte durée a été mis en évidence chez d. Pulchellus en réponse aux kairomones de contact de l'hôte. Enfin, le maintien de d. Pulchellus au laboratoire sur des hôtes issus d'un milieu artificiel pauvre en substances du poireau semble avoir sélectionné au bout d'une vingtaine de générations des parasitoïdes dont les stades larvaires sont plus sensibles aux allelochimiques du poireau.
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Ali, Magdi Mahmoud M. "The immunologic aspects of the pathogenesis of human onchocerciasis /." Stockholm : Dept. of immunology, Wenner-Gren institute, Stockholm university, 2006. http://urn.kb.se/resolve?urn=urn:nbn:se:su:diva-793.
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Jemli, Mohamed Habib. "Fasciolose ovine à Fasciola hepatica : contribution à son étude immunologique et biochimique." Toulouse, INPT, 1991. http://www.theses.fr/1991INPT015A.
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L'auteur etudie la fasciolose a fasciola hepatica chez le mouton, dans le double but de mieux connaitre la physiopathologie de la maladie et d'obtenir des moyens de diagnostic precoces et fiables. Apres un rappel concernant la maladie et ses consequences pathologiques et immunitaires, l'auteur presente les methodes d'etude puis les resultats obtenus chez des moutons infestes experimentalement par 200 metacercaires de grande douve en infestation unique. Il rapporte les perturbations immunologiques et biochimiques observees au cours de cette infestation, en remarquant surtout une augmentation importante dans le sang du nombre d'eosinophiles et des activites enzymatiques de la gldh et de la ggt. Leurs evolutions apres l'infestation refletent une atteinte hepatique sevissant entre deux phases successives (atteinte du parenchyme puis atteinte des canaux biliaires). Quelques enzymes tissulaires hepatiques (p-450 et les n-demethylases) ont ete aussi perturbes. Le traitement fasciolicide, par du triclabendazole, est efficace et permet la normalisation, en quelques semaines, des valeurs de parametres sanguins. Quatre reactions serologiques (elisa, immunofluorescence indirecte, hemagglutination passive et double diffusion sur gelose) sont comparees au cours de l'infestation. L'elisa s'est avere le meilleur moyen pour realiser des depistages de groupe ou lors d'enquetes epidemiologiques. L'hap est plus adaptee, pour etablir un diagnostic de la fasciolose de cas isoles. Une application sur le terrain, evoquant les caracteristiques epidemiologiques de la fasciolose ovine dans une region en tunisie, termine ce travail
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Marche, Hélène. "Etude de l'interférence d'une épi-drogue sur l'expression génique et la croissance intracellulaire de Toxoplasma gondii." Thesis, Université Grenoble Alpes (ComUE), 2019. http://www.theses.fr/2019GREAV019/document.
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Toxoplasma gondii est un parasite protozoaire intracellulaire obligatoire, et est l’agent responsable de la toxoplasmose, une parasitose habituellement bénigne chez le sujet immunocompétent ou en dehors d'une grossesse. Lorsqu’elle est congénitale, la toxoplasmose peut se manifester par de malformations neurologiques sévères. Cette maladie se développe sous deux formes. La première comprend à la phase aigüe provoquée par l’expansion de la population de tachyzoites qui peuvent provoquer des malformations chez le fœtus. La seconde est dite chronique et asymptomatique, le bradyzoite est y présent sous forme de kystes. Une réactivation des bradyzoites en tachyzoites peut être fatale pour les patients immunodéprimés. L’interconversion tachyzoïte-bradyzoïte est donc au centre de la pathogénèse de cette zoonose. L’interconversion est régulée au niveau transcriptionnel, avec un contrôle épigénétique strict. In vitro, il a été montré que l’inhibition de l’histone déacétylase TgHDAC3 par FR235222 induit la conversion. Dans cette thèse, nous avons étudiés un nouveau composé I2, ayant des propriétés agissant également sur les HDACs. Nous démontrons que ce composé inhibe la croissance chez toutes les souches de T. gondii, sans pour autant induire la différenciation tachyzoïte-bradyzoïte. Par contre, le composé I2 induit une déformation de la vacuole, qui prend l’apparence d’une bulle, uniquement chez certaines souches de T. gondii. D’après les expériences effectuées la distorsion de la vacuole n’interfère ne s’apparente pas à une paroi kystique. Un criblage génétique a permis de définir une région génomique responsable du phénotype « bulle » de la vacuole. En l’état actuel le gène responsable reste à être identifié ainsi que les mécanismes qui participent à la distorsion de la vacuole. Parallèlement, un autre projet a été initié sur la base d’une étude de gènes impliqués dans la croissance et/ou dans la résistance à l’IFNγ, cytokine principale de défense contre le parasite. Un gène a été étudié. La délétion de ce celui-ci chez le parasite provoque un défaut de croissance et de manière surprenante une résistance à un traitement à l’IFNγ. Ce gène et son mode de fonctionnement restent à être étudié. Ensemble, ces travaux nous montrent une adaptation de T. gondii à son environnement et le développement de mécanismes de survie qui restent à être élucidésToxoplasma gondii is an obligate intracellular protozoan parasite, and is the causative agent of toxoplasmosis, a benign parasitosis in immunocompetent or non-pregnant subjects. When congenital, toxoplasmosis can manifest as severe neurological malformations. This disease develops in two forms. The first includes the phase caused by the rise of the population of tachyzoites that can cause malformations in the fetus. The second is chronic and asymptomatic, bradyzoite is in the form of cysts. Reactivation of bradyzoites into tachyzoites may be fatal for immunocompromised patients. Tachyzoite-bradyzoite interconversion is therefore at the center of the pathogenesis of this zoonosis. Interconversion is regulated at the transcriptional level, with strict epigenetic control. In vitro, inhibition of histone deacetylase TgHDAC3 by FR235222 has been shown to induce conversion. In this thesis, we have studied a new compound I2, with properties that also act on HDACs. We demonstrate that this compound inhibits growth in all T. gondii strains, but does not induce tachyzoite-bradyzoite differentiation. On the other hand, the compound I2 induces a deformation of the vacuole, which takes the appearance of a bubble, only in certain strains of T. gondii. From the experiments carried out the distortion of the vacuole does not interfere with a cystic wall. Genetic screening has defined a genomic region responsible for the bubble phenotype of the vacuole. In the current state the responsible gene remains to be identified as well as the mechanisms that participate in the distortion of the vacuole. In parallel, another project was initiated on the basis of a study of genes involved in the growth and / or resistance to IFNγ, the main cytokine of defense against the parasite. A gene has been studied. The deletion of this one in the parasite causes a growth defect and, surprisingly, resistance to treatment with IFNγ. This gene and its mode of operation remain to be studied. Together, these works show us an adaptation of T. gondii to its environment and the development of mechanisms of survival that remain to be elucidated
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Israelsson, Elisabeth. "The role of antibody mediated parasite neutralization in protective immunity against malaria." Licentiate thesis, Stockholm University, Wenner-Gren Institute for Experimental Biology, 2007. http://urn.kb.se/resolve?urn=urn:nbn:se:su:diva-7137.
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Huppé, Vicky. "Analyse de l'eau de sources naturelles en régions éloignées et étude de gènes conservés dans l'évolution des parasites protozoaires retrouvés dans l'eau." Thesis, Université Laval, 2009. http://www.theses.ulaval.ca/2009/26419/26419.pdf.
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Mounkassa, Jean-Bruno. "Compétition interspécifique Schistosome-Echinostome chez le Mollusque vecteur : approche immunologique des mécanismes de compétition." Montpellier 2, 1987. http://www.theses.fr/1987MON20185.
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Etude de la competition larvaire entre schistosome et echinostome chez les mollusques hotes-intermediaires. Les resultats mettent en evidence une dominance totale de l'echinostome sur le shistosome dans toutes les situations experimentales testees (infestations mixtes simultanees, infestations mixtes decalees). Cette dominance est caracterisee par une inhibition du developpement larvaire du schistosome suivie d'une degenerescence totale des stades larvaires. L'analyse des mecanismes de competition a revele que la dominance de l'echinostome est mediee par le systeme immunitaire de l'hote
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Yilma, Jobre Makonnen. "Contribution à l'étude de l'épidémiologie, du diagnostic immunologique et de la physiopathologie de l'oestrose ovine (oestrus ovis linne 1761)." Toulouse, INPT, 1992. http://www.theses.fr/1992INPT036A.
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Une etude epidemiologique effectuee dans le sud-ouest a revele une prevalence elevee de l'infestation par oestrus ovis. L'evolution larvaire qui est fonction de la temperature exterieure et du niveau de precipitations, comprend une courte phase estivale de developpement actif et une phase prolongee d'inhibition hivernale. Des essais d'infestations experimentales ont confirme l'influence des facteurs climatiques sur la dipause. Dans une etude de simulation de l'strose par des transplantations larvaires repetees, des resultats ante mortem et post mortem significativement differents ont ete observes entre les animaux infestes et les temoins. La faiblesse du taux de recolte larvaire est du principalement a la grande mortalite des larves resultant de la reaction de l'hote. Un test de depistage par elisa a ete mis au point, les reactions optimales, hautement reproductibles et specifiques ont ete obtenues avec l'ag 20% de 2eme stade a 2 microgrammes de proteines par millilitre, avec des dilutions de serum et de peroxydase de 1/200 et 1/1000. F. Hepatica et h. Contortus n'ont presente aucune reaction croisee avec oestrus ovis. Des le septieme jour apres l'infestation unique, une augmentation du taux d'anticorps circulants a ete notee. Lors de l'infestation repetee, une chute initiale a ete suivie cinq semaines apres, par une augmentation spectaculaire. Des differences significatives de taux ont ete observees entre des groupes de moutons d'ages varies soumis a des infestations naturelles. Une cinetique bimodale de la population d'eosinophiles est la caracteristique de l'infestation unique. Une sensibilisation par des antigenes larvaires a declenche une reaction fugace, mais identique qu'avec des larves vivantes. L'effet mediateur des eosinophiles, par degranulation au contact de la larve semble etre le mecanisme principal de la reaction de l'hote. La reaction d'hypersensibilite immediate associee a cette infestation serait modulee par les produits des granules des eosinophiles
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Åhlin, Erik. "Functional Role of Immune Complexes in Rheumatic and Parasitic Diseases." Doctoral thesis, Uppsala universitet, Klinisk immunologi, 2011. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-139529.
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Immune complexes (IC) have key pathological roles in both autoimmune and infectious diseases. In this thesis functional mechanisms behind IC-driven inflammation in rheumatic diseases and tropical infections have been studied, with special focus on the contribution of autoantibodies and cytokine-inducing properties of IC. In the autoimmune disease SLE, increased levels of IC-induced cytokines were associated with both increased classical complement activation and the occurrence of the autoantibodies anti-SSA and anti-SSB, both directed against RNA-associated antigens. In addition, complement activation and anti-SSA synergistically predisposed to higher levels of IC in sera. In the following study it was demonstrated that also other autoantibodies against RNA-associated autoantigens were more enriched than anti-dsDNA in SLE IC. Sudanese Visceral Leishmaniasis (VL) patients had elevated IC levels, and precipitated IC induced higher levels of GM-CSF, IL10, IL6 and IL1RA than control IC. Levels of IC were especially prominent in severely ill patients receiving antimony treatment, and a parallel association with IC induction of GM-CSF was demonstrated. Leishmania-infected patients were often rheumatoid factor (RF) positive and a substantial number displayed reactivity towards cyclic citrullinated peptide (CCP) antigens. Contrary to what was seen in Sudanese RA sera, the CCP reactivity was not restricted to citrulline but reacted equally well with arginine-containing control peptides. Levels of anti-CCP among VL patients were not due to cross-reactions with, or CCP-reactivity bound to IC. I have demonstrated that IC are associated with the presence of autoantibodies in both SLE and in Leishmania infection. In SLE, autoantibodies against RNA-associated antigens were more prone to form circulating IC than anti-dsDNA. In Leishmania infection false reactivity against the CCP-autoantigen correlated to IC levels although the IC themselves did not contain such reactivity. In both diseases higher IC levels were associated with a more active disease, and purified IC induced key cytokines in disease pathogeneses.
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Rezvan, Hossein. "Studies on immunology of Leishmania mexicana." Thesis, Nottingham Trent University, 2007. http://irep.ntu.ac.uk/id/eprint/181/.
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Leishmaniasis is a worldwide disease prevalent in many tropical and sub tropical countries. Treatment of Leishmaniasis by chemotherapy is not wholly effective and is usually accompanied by unpleasant side effects. The development of an effective and inexpensive vaccine represents a practical way to control the disease, however at present no safe and effective vaccine is available. In the first part of the present study, the immunity induced by four different L. mexicana potential vaccines, including killed leishmania vaccine, Soluble L. mexicana Antigen (SLA), L. mexicana gp63 cDNA and CT26 tumour cells transfected with L. mexicana gp63, were compared. It was shown that DNA immunisation using L. mexicana gp63 generated the highest immunity to the parasite among the four tested vaccines where the killed leishmania vaccine and L. mexicana gp63 transfected CT26 tumour cells did not generate significant immunity. The efficacy of DNA immunisation by intramuscular injection or using gene gun, in generating immunity to leishmania was compared. Gene gun immunisation induced more immunity to the parasite and high levels of Th1 immune response, which were detected, one week after immunisation through determination of the IgG2a levels in blood serum. Gene gun immunisation also induced long-lasting CTL activity, which was detectable before and during the course of infection for up to 6 months. Immunogenicity of MHC class I restricted peptides derived from L. mexicana gp63 have been investigated. Using 'SYFPEITHI' software, four peptides with high affinity to human HLA-A2 and four peptides with high affinity to mouse H2-Ld were predicted, synthesized and tested in HHD II and BALB/c mice respectively. Only three of the peptides predicted with high affinity to HLA-A2 were immunogenic but only two of them were likely to be naturally processed, however, none were protective in HHD II mice against leishmania infection. Purification and application of OX40L, a ligand for T-cell co-stimulatory receptor, was investigated in L. mexicana BALB/c model. In addition to purification by protein A sepharose, the murine OX40L-IgG fusion protein produced by B9B8E2 cells (cells transfected with OX40L and IgG) was successfully purified by two novel resins, MBI & MEP. The biological activity of the OX40L-IgG purified by MBI resin was significantly higher than that of MEP or protein A sepharose resins. Application of OX40L-IgG resulted in healing of leishmania lesions or delaying in development of the lesions in leishmania-infected mice.
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Davis, Richard Elliot. "Neutrophil responses to infection with leishmania parasites: MHC class II-expression and parasite life-stage interactions." Diss., University of Iowa, 2016. https://ir.uiowa.edu/etd/2200.
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The vector-borne protozoan Leishmania spp. cause the spectrum of disease known as leishmaniasis in human and animal hosts. The most common manifestations of leishmaniasis are the chronic, ulcerative skin disease cutaneous leishmaniasis (CL), and the more serious visceral leishmaniasis (VL) in which parasites take up residence in internal organs, causing death if not treated. The role of neutrophils (PMNs) in the immune response to CL and VL is unclear. It is s generally thought that PMNs are only a short-lived effector cell, and have been disregarded as playing a role in chronic Leishmania spp. infection. As both CL and VL are diseases characterized by increased inflammatory immune mediators, we hypothesized that PMNs from human or animal models of chronic leishmaniasis would display different properties from PMNs from healthy controls. We found in a subset of CL and VL patients circulating PMNs expressing HLA-DR, the human form of MHC class II, a molecule thought to be restricted primarily to professional antigen cells. When we examined PMNs recruited to CL skin lesions in human patients, or similar lesions in experimental murine model of CL, we found significantly increased MHC class II+ PMNs. Circulating HLA-DR+ PMNs also expressed the co-stimulatory molecules CD80, CD86 and CD40. While this suggested an antigen-presenting cell-like phenotype by these HLA-DR+ PMNs, compared to conventional HLA-DR- PMNs, HLA-DR+ PMNs showed not only a neutrophil-like appearance and function, but in fact increased activation, degranulation, intracellular MPO and phagocytosis of parasites and zymosan particles. Incubation of healthy control whole blood with inflammatory cytokines resulted in increased HLA-DR+ PMNs and the presence of hladrb1 mRNA, suggesting a connection between neutrophil “priming” and upregulation of HLA-DR.
In addition to HLA-DR+ PMNs in CL patients, we also identified the presence of so-called “low-density” neutrophils (LD-PMNs). These neutrophils, which are enriched in low-density fractions following centrifugation of blood over a density gradient, are reported in numerous disease states, including cancer, HIV, and systemic lupus erythematosus. In some disease states, LD-PMN are reported to be immunosuppressive toward T cell activation and proliferation. However, LD-PMNs from leishmaniasis patients showed no evidence of immunosuppression. Additionally, we found that LD-PMNs show significantly increased surface expression of MHC class II, suggesting a heretofore unappreciated connection between these atypical neutrophil phenotypes. We also investigated the in vitro interactions with different Leishmania infantum life-stages, both those that cause acute infection (promastigotes) and amastigotes, which are found during chronic stages of the disease. We found that PMNs are readily infected by all L. infantum life-stages, but that amastigotes may have different methods of interacting with PMN surface receptors and are better equipped to avoid PMN anti-microbial responses.
These data suggest that circulating PMNs in chronic leishmaniasis may have unique phenotypes and interact differently with the Leishmania spp. life-cycle present during chronic infection. Further investigation of the role of PMNs and atypical PMN phenotypes in chronic disease may help identify new immunomodulatory roles for this cell type.
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Lellouche, Eric. "L'immunité locale dans deux parasitoses oculaires, toxoplasmose et onchocércose." Paris 5, 1993. http://www.theses.fr/1993PA05P084.
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Jeneby, Maamun. "Haemoprotozoan Parasites of Non-Human Primates in Kenya : Studies on Prevalence and Characterization of Haemoprotozoan Parasites of Wild-Caught Baboons, African Green Monkeys and Syke's Monkeys." Doctoral thesis, Uppsala universitet, Försöksdjursvetenskap, 2011. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-150467.
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This thesis reports on cross-sectional surveys aimed at detecting and characterizing haemoprotozoan parasites infecting wild free-ranging non human primates (NHPs) in Kenya, East Africa. Blood samples from olive baboons (Papio cynocephalus anubis), vervet monkeys or African green monkeys (AGMs, Chlorocebus aethiops) and Syke's monkeys (Cercopithecus mitis) from five provinces of Kenya were analyzed. The haemoprotozoan parasites survey was performed with microscopic evaluation of blood smears, serological techniques and molecular tools. Blood specimens and serum samples from 121 NHPs were tested for the presence of Trypanosoma brucei (Study I). Indirect antibody enzyme-linked immunosorbent assay (Ab-ELISA) detected titers of anti-T. brucei antibodies in 19% (23/121) of the sera sampled. Subsequent field-oriented latex agglutination test (LAT) detected presence of T. brucei antigens in 16% (19/121) of the sera. However, there were no active infections detected on fixed blood smears, or wet blood films. Of the 378 NHPs sera samples tested for Leishmania major exposure using Ab-ELISA, 66% had detectable anti-L. major antibodies (study II). Western blot (WB) assay detected anti-L. major antibodies in sera from 46% (175/378) of the NHPs samples. Specific proliferation of peripheral blood mononuclear cells to L. major antigen was demonstrated in 23% (17/57) of AGMs samples. Haemoprotozoan parasites, Entopolypoides macaci and Hepatocystis kochi were detected by microscopic evaluation of Giemsa-stained blood smears from 179 NHPs (study III). The prevalence rate of E. macaci was 43% in African green monkeys, 35% in Syke’s monkeys and 33% in baboons. H. kochi infection rate was 18% in African green monkeys, 23% in baboons and 25% in Syke’s monkeys. Subsequent indirect immunofluorescent antibody test (IFAT) supported the morphologic appearance of E. macaci observed by microscopy. Molecular tools were used to detect and identify haemoprotozoan parasites in wild free-ranging NHPs (study IV). Nested polymerase chain reaction (PCR) targeting Babesia β-tubulin gene detected a 22% (27/125) B. microti infections in free-ranging NHPs in Kenya. PCR also detected 22% mixed infections by Hepatocystis and Entopolypoides, 12% Hepatocystis and Babesia and 7% Entopolypoides and Babesia (study V). Phylogenetic analysis inferred from mitochondrial cytochrome b (Cyt-b) gene confirmed the presence of Hepatocystis kochi whereas analysis of 18SS rRNA gene confirmed presence of two piroplasms, Babesia sp. and Entopolypoides macaci. In conclusion, epidemiological results from sero-prevalence studies provide strong circumstantial evidence that some species of Kenyan NHPs are naturally exposed to L. major and T. brucei infections and could be potential reservoir hosts for these haemoparasites. Molecular diagnosis revealed the occurrence of mixed parasite infections and confirmed the circulation of Babesia and Entopolypoides species in the same populations of Kenyan NHPs.
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Geoffroy, Patrick. "Place du granulome bilharzien dans l'interaction immunologique parasite hôte chez "Schistosoma mansoni"." Paris 5, 1990. http://www.theses.fr/1990PA05P240.
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Mohammed, Shawn Rasheed. "Disaccharidase deficiencies in gerbils (Meriones unguiculatus) immune to Giardia lamblia." Thesis, McGill University, 1994. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=55514.
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Studies using Mongolian gerbils found that during a primary infection with Giardia lamblia trophozoites, disaccharidase activities were decreased from day 10 post-infection (p.i.) until well past elimination of the parasite. However, during a challenge infection, enzyme deficiencies were short-lived. A challenge with a soluble extract of G. lamblia trophozoites also resulted in reductions in disaccharidase activity. The degree of these reductions in enzyme activity was dependent on the extract dose. Gel filtration of the trophozoite crude extract resulted in fractions F1, F2, and F3. However, only a challenge with F1 led to disaccharidase deficiencies. Further separation of F1 resulted in fractions F1a and F1b. Impairments of enzyme activity were obtained only in gerbils challenged with F1b. Protein analysis of F1b revealed several high and low molecular weight bands. When gerbils previously exposed to G. lamblia were challenged with an extract of Entamoeba histolytica trophozoites, disaccharidase activities remained comparable to controls. Moreover, enzyme levels in gerbils challenged with excretory/secretory G. lumblia products were affected in a manner which was inconsistent with the live parasitic challenge. Results suggest that the disaccharidase deficiencies in giardiasis are parasite-specific and are induced by a heat-stable constituent(s) of fraction F1b, possibly through an immune response to an antigenic component of this parasite fraction.
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Anderson, Barry Clayton. "The Response of Mice to Infection by the Parasitic Nematode Trichinella: A Comparison of Trichinella Spiralis and Trichinella Pseudospiralis." PDXScholar, 2002. https://pdxscholar.library.pdx.edu/open_access_etds/1658.
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The intracellular parasite Trichinella is a genus in phylum Nematoda that contains six named species including Trichinella spiralis and Trichinella pseudospiralis. These parasites infect a large variety of wild and domestic animals, human beings and a few species of birds. The parasitic strategies and the pathological effects on the host between trichinella spiralis and Trichinella pseudospiralis are quite different.
The purpose of this study is to gain an understanding of the physiological, immunological and pathological differences between these two species of Trichinella using infections in the mouse as a model. In the course of this research I have attempted to answer the following questions: A) Is cortisol a factor in the differences of the host response to Trichinella spiralis or Trichinella pseudospiralis? B) Are there differences in leukocyte response in the peripheral blood of Trichinella infected mice? C) Are there differences in the up-regulation or down-regulation of cell surface molecules on leukocytes in the spleens of Trichinella infected mice? D) Is there a difference in the degree of muscle damage (as measured by creatine phosphokinase) when infections by the two species of Trichinella are compared? E) Are there differences in angiogenesis and collagen deposition in Trichinella infected mice and are these differences related to cortisol? F) Is nitric oxide a component in parasite killing and are there differences in nitric oxide production in host mice when the two species of Trichinella are compared?
My research has shown that there are significant differences in the parasitic strategies and pathological consequences in mice infected with one or the other of the two species of Trichinella. The two species appear to generate different immune and inflammatory responses from the host. Trichinella pseudospiralis is much less damaging to the host, generates a very different peripheral blood response, stimulates the production of substantially greater levels of serum cortisol, generates a significantly different profile in cytokine production presents a very different cell surface antigen profile and does not produce a collagen nurse cell or generate an angiogenic response when compared to T spiralis. In addition, I have shown a role for nitric oxide in parasite killing and a role for serum cortisol in larval survival. I have also shown that cortisol has no role in either collagen deposition or the angiogenic response in Balb/c mice under the experimental conditions detailed here.
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McSorley, Henry. "TGF-β homologues from parasites : inducers of immune regulation?" Thesis, University of Edinburgh, 2008. http://hdl.handle.net/1842/3157.
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Many helminth parasites are able to survive for long periods in immunocompetent hosts. It has been suggested that the successful establishment of helminths is in part due to the induction of regulatory T cells (Tregs) which suppress anti-parasite immune responses. A possible mechanism by which parasites induce Tregs would be production of TGF-β, which can induce immunosuppressive Treg cells and also directly suppress immune responses. TGF-β homologues have been identified in parasitic nematodes including Brugia malayi, Schistosoma mansoni and Ancylostoma caninum. The B. malayi TGF-β homologue, Bm-TGH-2, has been demonstrated to signal through the mammalian TGF-β receptor, which indicates the TGF-β homologues may have a function in the host. We hypothesised that Treg induction through parasite-derived TGF-β could be a potent method by which parasites could evade the host immune system. To address this, molecular techniques were first used to identify and characterise the transcription of novel TGF-β homologues from the intestinal parasites Haemonchus contortus, Heligmosomoides polygyrus, Nippostrongylus brasiliensis and Teladorsagia circumcincta, showing that TGF-β homologues are present in a wide range of parasites. TGF-β activity was then shown in products from both S. mansoni and H. polygyrus, and indeed the H. polygyrus products were found to induce Tregs through the TGF-β pathway. Antiserum against bacterially expressed H. polygyrus TGF-β homologue (Hp-TGH-2) was produced, and used to probe H. polygyrus excretory/secretory products, showing that Hp-TGH-2 is secreted. Attempts were also made to express recombinant Bm-TGH-2 (B. malayi TGF-β homologue) in insect cells, however the purified protein proved not to be functional. - v - In vivo mouse models of B. malayi infection were tested to examine the phenotype of T cell responses at the site of infection. An accumulation was found of CD4+Foxp3+CD25+CTLA-4hiCD103+ T cells, which resemble activated natural Tregs, and which were suppressive in vitro. This proportion of Tregs at the site of infection diminishes over time, however CD103 expression (which is associated with activated Tregs) is increased on Tregs present at all timepoints up to day 21 postinfection, indicating that although a growing effector response may outgrow Tregs over time, the Treg population remains activated. Using an adoptive transfer model, it was shown that the Treg induction could spread to other bystander responses. In IL-4R-deficient mice, Treg accumulation was unaffected, indicating alternatively activated macrophages (which are absent in these mice) are not required for Treg induction.
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Contreras, Garcia Irazú. "Modulation of the host innate immune response by «Leishmania» parasites." Thesis, McGill University, 2010. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=95096.
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Leishmania parasites have evolved sophisticated mechanisms to subvert macrophage immune responses in order to survive inside the mammalian host. Among these mechanisms are the rapid activation of phosphatases that in turn will inactivate protein kinases and transcription factors, causing abrogation of nitric oxide (NO) production and induction of immunosuppressive molecules. This doctoral thesis discusses novel mechanisms of how the parasite modulates the immune response of macrophages and dendritic cells. Herein, we describe the role of Myeloid Related Proteins (MRPs) 8 and 14 during Leishmania infection. MRPs 8/14 are produced by neutrophils and are able to induce microbicidal activity in macrophages. We present data that shows that priming macrophages with MRP 8/14 before infection induces their activation. However, infection with L. major prior to MRP stimulation significantly decreases their activation. In vivo studies showed that abrogation of MRPs resulted in an increased parasitic burden, whereas injection of recombinant MRPs (rMRPs) reduced the size of the lesion and the parasitic load. One of the main mechanisms that Leishmania parasites utilize to subvert the innate immune response is the alteration of transcription factors (TFs). In this thesis, we have shown that upon Leishmania infection, AP-1 activity is abolished and this correlates with the nuclear degradation of AP-1 subunits. Of interest, c-Jun, the main AP-1 activator is degraded and cleaved by Leishmania inside the nucleus in a GP63 dependent manner. Despite the fact that macrophages have been considered as preferred hosts for Leishmania parasites, other cells have been described as possible hosts. Finally, we discuss the effect of Leishmania infection in dendritic cells (DCs) and how this pathogen affects their maturation and capacity to present antigen. In addition, we found that Leishmania is able to activate phosphatases to inactivate signalling pathways in these cells. Collectively, oLe parasite Leishmania a su développer des mécanismes sophistiqués lui permettant de déjouer les réponses immunitaires des macrophages dans le but de survivre à l'intérieur de son hôte mammifère. Parmi ces mécanismes, notons l'activation rapide de phosphatases, qui inactiveront des protéines kinases et des facteurs de transcription, causant ainsi l'abrogation de la production d'oxyde nitrique, de même que l'induction de molécules immunosuppressives. Cette thèse doctorale discute de nouveaux mécanismes utilisés par le parasite afin de moduler la réponse immunitaire des macrophages et des cellules dendritiques. Dans le présent rapport, nous décrirons le rôle des MRPs (Myeloid Related Proteins) 8 et 14 lors de l'infection par Leishmania. Produites par les neutrophiles, les MRPs 8/14 ont la capacité d'induire l'activité microbicide des macrophages. Nos résultats montrent qu'une sensibilisation active pré-infection des macrophages avec les MRPs 8/14 induit leur activation. Par contre, lorsque l'infection à L.major est antérieure à la stimulation avec les MRPs, l'activation des macrophages est significativement réduite. Les études in vivo démontrent quant à elles que l'abrogation des MRPs a entraîné une augmentation de la charge parasitaire, alors que l'injection de MRPs recombinantes réduit la taille de la lésion, de même que la charge parasitaire. Un des principaux mécanismes qu'utilisent les parasites Leishmania, afin de déjouer la réponse immunitaire innée, est l'altération de facteurs de transcription. À l'aide de nos résultats, nous démontrons que l'activité d'AP-1 est abolie suite à l'infection par Leishmania, ceci concordant avec la dégradation au noyau des protomères d'AP-1. Il est d'ailleurs à souligner que c-Jun, le principal activateur d'AP-1, est dégradé et clivé par Leishmania à l'intérieur du noyau, et ce de façon GP63 dépendante. Malgré le fait que les macrophages sont considérés comme les cell
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Missoh, Claudia. "Division of labor in anti-parasite defense strategies in ant colonies." Thesis, Paris 6, 2014. http://www.theses.fr/2014PA066450/document.
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La division du travail est une caractéristique clé chez les insectes sociaux et contribue à leur succès écologique. En ce qui concerne les tâches sanitaires, la division du travail au sein d’une colonie peut permettre de réduire la transmission des maladies, de libérer certaines ouvrières pour d’autres tâches, permettant de diminuer les couts associés à l’exécution des tâches sanitaires (sur le plan comportementale et physiologique). Les facteurs externes et internes aux individus déterminant leur participation aux tâches sanitaires ne sont pas bien connus. La plupart des études portent sur l’importance des différences génétiques entre ouvrières. Dans les deux premières études, j’ai examiné le rôle de l’expérience des individus (par exposition répétée à des déchets sanitaires ou à l’exécution d’une tâche) sur la mise en place de différences interindividuelles dans l’exécution d’une tâche sanitaire comportementale. L’exposition à un parasite est une menace fréquente au sein de colonies d’insectes sociaux. En utilisant la fourmi clonale Platythyrea punctata, j’ai voulu savoir si une exposition répétée des individus à des larves portant une faible quantité de conidiospores du champignon Metarhizium robertsii affectait la performance des soins sanitaires portés au couvain. J’ai trouvé que la durée de nettoyage des larves était plus élevée chez des fourmis entrainées, aux larves exposées ou non exposées au champignon, que chez des fourmis inexpérimentées. Un temps de nettoyage plus élevé améliorait l’élimination des conidiospores. Ainsi les fourmis entrainées pourraient être plus efficaces pour éliminer les conidiospores lors d’une attaque parasitaire de la colonie. La décomposition des cadavres représente un risque sanitaire dans les colonies d’insectes sociaux, nécessitant une gestion de cadavres. Dans la deuxième étude, j’ai étudié la possibilité d’une division du travail dans la gestion des cadavres (c'est-à-dire le nettoyage et le transport) chez les ouvrières de la fourmi polygyne et polymorphe Cataglyphis velox. J’ai plus spécifiquement testé si la propensité d’accomplir ces tâches était en rapport avec une récente expérience individuelle ou avec la taille des ouvrières. Nos observations ont montré que la majorité des individus de la colonie n’effectuait que rarement des tâches de gestion de cadavres même si quelques individus pouvaient être impliqués plus fréquemment, au moins sur un laps de temps cours, dans l’exécution de ces tâches. Les résultats suggèrent une faible division du travail dans le nettoyage et le transport des cadavres et une faible modulation de ces tâches par l’exposition répétée des ouvrières à des cadavresDivision of labor is a key characteristic of social insects and contributes to their ecological success. Especially in disease defense, the intra-colony partitioning of sanitary work can reduce disease transmission, keep nestmates available for other tasks and reduce costs associated with sanitary task performance (i.e. at the behavioral and physiological level). Factors internal and external to the individual affecting sanitary task allocation are not well known and most studies investigated genetic differences between workers performing behavioral sanitary work. In the first two studies I addressed whether individual experience (through repeated exposure to a sanitary hazard or performance of the task) can generate interindividual differences in the performance of behavioral sanitary tasks. Repeated parasite exposure is a common threat in colonies of social insects, posing selection pressures on colony members to respond with improved disease-defense performance. In the clonal ant Platythyrea punctata, I tested whether experience gained by repeated tending of low-level fungus-exposed (Metarhizium robertsii) larvae alters the performance of sanitary brood care. I found that ants trained both with sham- and fungus-treated larvae groomed the brood longer than naive ants. Increased grooming of fungus-treated larvae resulted in more effective fungal removal, thus making trained ants better caretakers under parasite attack of the colony. Decomposing cadavers pose a sanitary risk to social insect colonies, necessitating cadaver management. In the second study I investigated whether cadaver management (i.e. cadaver grooming and transports) is divided among workers and task allocation affected by recent individual experience or worker size in the polymorphic and polygynous ant Cataglyphis velox. Many individuals performed cadaver management infrequently and few individuals dominated task performance. Our results suggested low division of labor for cadaver grooming and transport and a reduced modulation of these behaviors by recurrent exposure to nestmate cadavers
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Baeza, Elisabeth. "Suivi de la réponse immunitaire précoce aspécifique chez le rat infesté expérimentalement par "Fasciola hepatica"." Montpellier 2, 1992. http://www.theses.fr/1992MON20261.
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Ce travail est une contribution a l'analyse des mecanismes immunitaires precoces qui se mettent en place au cours d'une infestation par f. Hepatica chez le rat. Apres la mise au point d'une technique d'infestation experimentale du rat, la repetabilite de ce type d'infestation a ete verifiee. Une etude de l'evolution de proteines de la reaction inflammatoire et des leucocytes au cours de la phase precoce de la fasciolose a montre une absence de modification de ces marqueurs de l'inflammation pendant les deux premieres semaines qui suivent l'infestation. L'immunomodulation de la reponse inflammatoire de l'hote, au moment de l'infestation, fait apparaitre: - le role essentiel du systeme inflammatoire pour limiter l'installation et le developpement des douves; une action anti-inflammatoire exercee par f. Hepatica au cours des deux premieres semaines d'infestation; une protection accrue de l'hote consecutive a l'administration de stimulants de l'inflammation de l'ordre de 40-50%. L'etude des interactions entre f. Hepatica et le complement, in vivo et in vitro, a mis en evidence une action depletive du parasite uniquement sur l'activite cytolytique de la voie classique
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Jacobs, Brittany-Amber. "Cancer cell behaviour following parasite exposure." Master's thesis, University of Cape Town, 2018. http://hdl.handle.net/11427/29273.
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Infectious diseases, including helminthiases, are estimated to cause 16.1% of global cancer cases. While certain helminths are conclusive causes of cancer, others have been shown to reduce the disease. It is currently unknown why differing helminth infections promote or prevent cancer development and progression, or which cellular mechanisms are altered following exposure. Using several in vitro and in vivo techniques, this study aimed to determine the effect that certain helminths have on the progression of cervical and colorectal cancer. The results revealed that antigen from the hookworm Nippostrongylus brasiliensis significantly reduced cervical cancer cell migration and the expression of two markers of metastasis: vimentin and N-cadherin. Importantly, N. brasiliensis antigen significantly lowered the expression of cell-surface vimentin, while decreasing Human Papillomavirus type16 pseudovirion internalization. In vivo infection with N. brasiliensis significantly decreased vimentin expression within the female genital tract, confirming the relevance of these in vitro findings. Furthermore, exposure to antigen from the gastrointestinal nematode Heligmosomoides polygyrus decreased the in vitro proliferation of human and mouse colorectal cancer cells and simultaneously increased the expression of cell cycle regulator proteins, p53 and p21. Surprisingly, while antigen from H. polygyrus inhibited human colorectal cancer cell migration, it had the opposite effect on mouse colorectal cancer cells, suggesting that its impact on colorectal cancer migration may be, at the very least, species dependent. Using a syngeneic tumour model, the excretory-secretory product from H. polygyrus was shown to significantly increase tumour growth and the expansion of regulatory T cells and neutrophils in the tumour. Similarly, in a model of colitis-associated colorectal cancer this antigen significantly worsened pathology in a TGF-β dependent manner. Undoubtedly, the knowledge gained from this study will contribute to the limited understanding about helminths and the effect that these parasites have on cancer progression.
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Anderson, Laura Fay. "Malaria proteins implicated in host-parasite interactions." Thesis, University of Edinburgh, 2007. http://hdl.handle.net/1842/1965.
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The invasive and transmission stages of the malaria parasite Plasmodium falciparum express several proteins with domains implicated in host-parasite interactions, that are potential vaccine candidates or drug targets. The expression patterns of two proteins PfTRAMP (Plasmodium Related Apical Merozoite Protein) and PCRAGS (Plasmodium cysteine related antigen of gametocytes and schizonts), containing such putative domains, are examined and their potential roles in merozoite invasion and egress are discussed. PfTRAMP has a possible role in merozoite invasion. Transcription occurs in mature schizonts as shown by Northern blot. Recombinant protein was successfully expressed in insect cells indicating that this eukaryotic system can be utilised for the expression of Plasmodium proteins. PCRAGS is a member of the Plasmodium Cysteine Repeat Modular Proteins (PCRMPs), a family of high molecular weight proteins with highly conserved, cysteine-rich regions and multipass transmembrane domains. The gene encodes a signal sequence, a truncated extracellular domain, an EGF-like domain and a multipass-transmembrane domain. PCRAGS is highly conserved in Plasmodium spp and other Apicomplexa. The extracellular domain has been under purifying selection, suggesting that the sequence or the structure of this domain is important for function. The gene is transcribed throughout the asexual erythrocytic cycle and is expressed in both gametocytes and schizonts in P. falciparum and in the rodent malaria P.berghei. Antibodies raised against a short peptide in the C-terminus detect PfCRAGS during schizont rupture and in mature segmenting schizonts but not in merozoites. Western blotting showed that PfCRAGS is present in the membrane fraction. Co-localisation studies showed that PfCRAGS is associated with the infected erythrocyte membrane, suggesting a role in merozoite egress. PfCRAGS is also expressed in stage II-IV male gametocytes in association with a membrane and is the earliest known male specific protein expressed. Gene knock-out of pbcrags in P. berghei showed that PbCRAGS is not essential for asexual development. In vivo evaluation of phenotype showed that pbcrags knock-out parasites are less virulent than wildtype parasites and have an increased gametocyte production in a non-susceptible host. The unique expression and localisation pattern of PfCRAGS in combination with putative host-parasite binding domains implicate this novel protein as a potential vaccine candidate or drug target.
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Ben-Smith, Anne. "Mechanisms of expulsion of primary infections of Heligmosomoides polygyrus in mice." Thesis, University of Nottingham, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.284027.
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Oldridge, Joanne. "Molecular and immunological characterisation of two vaccine dominant antigens of Schistosoma mansoni." Thesis, London School of Hygiene and Tropical Medicine (University of London), 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.307435.
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Bartley, Paul Murdoch. "Host-parasite interactions of Neospora caninum." Thesis, University of Edinburgh, 2017. http://hdl.handle.net/1842/23592.
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The papers included in this thesis examine the host–parasite relationship in small and large animals following experimental challenges with Neospora caninum. This apicomplexan parasite is a major cause of abortion and reproductive losses in cattle worldwide. Economic and welfare issues make the development of a vaccine against the transplacental transmission of Neospora highly desirable. This thesis evaluates the host-parasite interactions in a non-pregnant mouse model examining whether the actively multiplying stage of the parasite (tachyzoite) could be attenuated through prolonged in vitro cultivation (passage) and used as a live vaccine. We show that continued maintenance of tachyzoites in tissue culture produced significantly reduced levels of morbidity and mortality in the mice following challenge, compared to mice receiving virulent parasites. Inoculation with a sub-lethal dose of tachyzoites was shown to protect against a subsequent lethal challenge of virulent parasites. Mice showing higher levels of cell mediated immunity (CMI) (antigen-specific splenocyte proliferation and interferon-γ (IFN-γ) production) had lower parasite burdens compared to mice with less pronounced CMI responses. Combined, these works show that it is possible to protect against a lethal challenge using attenuated tachyzoites and that a strong T-helper Type-1 CMI response is involved in protection and in reducing clinical disease severity. As the most commonly known route of infection with N. caninum is transplacental, from dam to foetus, we also wanted to examine the host-parasite relationship in pregnant cattle. This was done through the serial examination of the maternal and foetal immune responses of experimentally challenged cattle under controlled conditions at different stages throughout pregnancy. These works show the importance of the timing, location and magnitude of multiple components of the host immune response in determining foetal survival and also whether vertical transmission occurs. We show that both the maternal and foetal immune responses are critical in determining the clinical outcome of infection. A strong maternal CMI response was shown to aid foetal survival by reducing the numbers of parasites reaching and thus damaging the placenta. Due to the syndesmychorial nature of the ruminant placenta, any foetal responses observed are as a result of foetal infection. These experiments show that as pregnancy progresses the foetus goes from being immunologically immature and incapable of mounting a protective immune response (70 days of gestation (dg)) to becoming capable of mounting parasite-specific humoral, innate and CMI responses from around 140dg onwards. The experiments in pregnant cattle confirm the importance of parasite-specific proliferation and IFN-γ production, in reducing the magnitude of the parasite challenge reaching the maternal–foetal interface and aiding foetal survival. We also examined the immunodominant parasite peptides expressed in HPLC fractionated tachyzoite antigen, which are recognised by the cellular immune response of experimentally challenged cattle. Through LC-ESI-MS/MS, 6 Neospora proteins (including SAG1, SRS2 and GRA2) and a number of Toxoplasma gondii orthologues were identified and found to be recognised by CD4+ T-cells. These works collectively demonstrate the complexity of the host-parasite interaction in Neospora infections and show the importance of a CMI response in protection against the parasite.
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THIAM, KADER. "Strategie de modulation de la reponse immune : du vecteur vivant au lipopeptide synthetique (doctorat : immunologie parasitologie)." Lille 2, 1999. http://www.theses.fr/1999LIL2T004.
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Jecock, Rowena M. "Studies on GP30 and other developmentally-regulated proteins of Brugia pahangi." Thesis, University of Liverpool, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.333555.
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Kadian, Surinder Kumar. "Immunoregulation in metacestode infections : modification of macrophage accessory activity by tetrathyridia of Mesocestoides corti." Thesis, University of Liverpool, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.240521.
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Pattaradilokrat, Sittiporn. "Linkage group selection to investigate genetic determinants of complex traits of malaria parasites." Thesis, University of Edinburgh, 2008. http://hdl.handle.net/1842/3139.
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Malaria parasites of the species infecting humans and animal hosts exhibit genetic and phenotypic diversity. Some of this diversity, including the responses to anti-malarial drugs, growth rate and virulence and antigenic variability, is medically significant. This is because these phenotypes may determine the existence and survival of the parasites in the host and, in turn, contribute to the clinical outcome of infection. Understanding of the biological characteristics and the genetic basis underlying these complex phenotypes can thus lead to the development of effective control strategies against the disease, such as anti-malarial drugs and vaccines. Genetic studies in rodent malaria parasites have proved useful in providing insights into the genetic determinants of these complex traits and thus can be used to complement the study of human malaria. The present studies aim to investigate genetic determinants underlying two major medically important phenotypes, Strain Specific Protective Immunity (SSPI) and Growth rate, using the newly devised genetic method of Linkage Group Selection (LGS). The results presented here relate to the accomplishment of these aims. LGS analysis of SSPI using a genetic cross between clones AJ and CB-pyr10 of Plasmodium chabaudi chabaudi has identified a single region on chromosome 8 containing the gene for the Merozoite Surface Protein-1 as encoding a major target of SSPI. A similar finding was also obtained in a previous LGS study using a different genetic cross between clones AS-pyr1 and CB of P. c. chabaudi (Martinelli et al., 2005). Hence, the results of two independent studies strongly indicate that a single locus within the parasite genome contains a major target antigen, or antigens, of SSPI against P. c. chabaudi malaria. These results have particular relevance for research on SSPI in human malaria and the choice of candidate antigens for malaria vaccine development. LGS analysis of growth rate conducted upon a genetic cross between a fast-growing line, 17XYM, and a slow-growing line, 33XC, of Plasmodium yoelii yoelii has identified a ~ 1 megabase pair region on P. y. yoelii chromosome 13 as containing a major genetic determinant(s) of growth rate in these malaria parasites. This is consistent with the finding of the classical linkage analysis by Walliker et al., (1976), that growth rate in P. y. yoelii is mainly determined at a single genetic locus. Because the fast-growing line 17XYM arose spontaneously during infection with a mild strain of P. y. yoelii 17X, identification of parasites with a slow growth rate phenotype derived from the same genetic stock as 17XYM can be useful in determining genes underlying growth rate in these malaria parasites. It has been shown here that parasites of the P. y. yoelii lines 17X consist of two completely distinct genotypes. One is represented by the fast-growing line, 17XYM, and a slow-growing line of P. y. yoelii, 17XNIMR. The other is represented by another slow-growing line 17XA. Comparing the region of P. y. yoelii chromosome 13 under strong growth selection between the two congenic lines, 17XYM and 17XNIMR, could lead to the identification of the gene(s) controlling growth rate differences in these two parasite lines. Such findings could be relevant to the location of genetic determinants of growth rate in human malaria.
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Bolad, Ahmed Kamal. "Antibody responses in Plasmodium falciparum malaria and their relation to protection against the disease." Doctoral thesis, Stockholm : Wenner-Grens institut, Univ, 2004. http://urn.kb.se/resolve?urn=urn:nbn:se:su:diva-37.
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Paterson, Jacqueline C. M. "Modulation of T cell responses by the products of Ascaris suum." Thesis, University of Glasgow, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.312783.
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Hayward, Adam David. "Parasites and life history variation in a wild mammal." Thesis, University of Edinburgh, 2011. http://hdl.handle.net/1842/5675.
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The purpose of this thesis is to investigate associations between parasite infection and host life-history variation in the wild Soay sheep population of the islands of St Kilda, NW Scotland. Studying host-parasite interactions in wild animal populations is of interest because of the importance of heterogeneity in resource availability, genetics, and environmental conditions in determining resistance to parasites, with implications for human populations and wildlife conservation and management. However, very few studies are able to investigate these associations in a longitudinal manner, which is essential in order to understand how infection is associated with life-history variation across ages and environmental conditions. In this thesis, I investigate associations between parasite resistance and ageing and the importance of maternal effects on offspring parasite resistance. I also establish the shape of natural selection on parasite resistance, and associations between measures of parasite burden and antibody responses. The principle findings of the analyses presented in this thesis are: i) Adult sheep of both sexes show a decline in parasite resistance in old age which is consistent with senescence. Furthermore, the rate of decline in parasite resistance with age is accelerated in individuals that have experienced more stressful environmental conditions over their lifespan. ii) Aspects of maternal phenotype and lamb early life performance are significantly associated with parasite resistance in lambs. Some of these effects persist into adult life and may even affect late-life changes in parasite resistance with age. iii) Analysis of ageing in five female reproductive traits shows that the contributions of individual senescence, terminal effects, and selective disappearance vary across traits, and that therefore multiple traits should be studied in order to understand ageing more fully. Most strikingly, there was no evidence for significant senescence in the probability of producing twins. iv) The first estimate of the strength of natural selection on parasite resistance in a longitudinally-monitored population provided evidence for positive selection on parasite resistance in lambs but not adults. Selection in lambs also varied across environmental conditions, being stronger in years of more favourable conditions. v) Analysis of associations between estimates of parasite burden and antibody responses showed that an estimate of parasite burden was not correlated with either a general or parasite-specific antibody response. However, antibody responses were positively correlated, and there was some evidence for a genetic correlation between the two in lambs but not adults.
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Steed, Lisa Lovett. "Host-parasite interactions between Bordetella pertussis and human polymorphonuclear leukocytes." Diss., The University of Arizona, 1991. http://hdl.handle.net/10150/185641.
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Little is known regarding the interaction of Bordetella pertussis with polymorphonuclear leukocytes (PMNL) or the role PMNL play as an initial line of defense against B. pertussis infection. An in vitro system was developed to establish optimum conditions for the study of phagocytosis and killing of three virulent strains of B. pertussis and a series of derivative mutants using strictly human PMNL and sera. Optimum phagocytosis of B. pertussis occurred by opsonization with human anti-B. pertussis antibody (HAPA), while autologous normal sera (NS) did not induce significant phagocytosis. An antiserum made in rabbits against an avirulent strain was required as an opsonin for significant phagocytosis of several avirulent strains. Over 50% of all B. pertussis strains and mutants tested survived PMNL bactericidal activities while Escherichia coli controls were readily killed. Therefore, if internalized, B. pertussis has an innate ability to survive within human PMNL. No one virulence factor appears to be superior to another in determining survivability. Electron microscopic studies using acid phosphatase as a lysosomal marker demonstrated that virulent B. pertussis strains are capable of surviving intracellularly within PMNL phagosomes and that such survival is due to inhibition of phagosome-lysosome fusion. PMNL respiratory burst activity is unaffected by internalized B. pertussis. This strongly suggests that inhibition of phagosome-lysosome fusion is the key mechanism of B. pertussis intracellular survival within PMNL.
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Yourth, Christopher Paul. "Ecological immunology of lestid damselflies, explaining variation in immune defense against parasitic water mites." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2001. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp05/MQ63244.pdf.
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Bucsu, Eva. "Plasmodium chabaudi adami : vaccine antigens and antigenic variation /." Connect to thesis, 2003. http://repository.unimelb.edu.au/10187/2881.
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There is an abundance of information available on the molecular mechanisms of antigenic variation in Plasmodium falciparum. The variant antigen PfEMP1, which mediates antigenic variation as well as cytoadherence and rosetting, has been extensively characterised. Genes coding for the antigen belong to the gene family var, and several var genes have been cloned and characterised. The rodent malaria parasite P. chabaudi is a widely studied in vivo model for P. falciparum. The P. c. chabaudi AS parasite strain has been shown to exhibit antigenic variation and the variant antigen has been detected by surface fluorescence. As with P. falciparum, there is a link between antigenic variation and cytoadherence, however genes coding for the variant antigen in P. chabaudi have not been cloned to date. Therefore, potentially useful in vivo experiments on antigenic variation are restricted. In this thesis it is shown for the first time that the P. c. adami DS parasite strain also exhibits antigenic variation.Chapter 3 describes efforts to locate genes coding for variant antigens in P. c. adami DS. The main strategy involved a genome survey, by sequencing and analysing randomly selected clones from a P. c. adami DS genomic library. DNA sequences were compared to Plasmodium spp. sequence databases to look for similarity to var genes or other genes encoding variant antigens. Of the 297 clones analysed none had significant sequence similarity to genes coding for variant antigens. However, in a small proportion of sequences some similarity to var genes was noted. Several genes of potential interest were identified, most importantly the gene coding for the vaccine candidate rhoptry associated protein 1 (RAP1), which was subsequently cloned and characterised. Further attempts to locate var gene homologues in P. c. adami involved amplification of P. c. adami genomic DNA using degenerate oligonucleotide primers corresponding to conserved regions of var genes. This strategy proved to be unsuccessful, most likely due to lack of sequence similarity between P. falciparum and P. c. adami genes. In several vaccination studies with the apical membrane antigen 1 (AMA1) of P. c. adami DS, mice were significantly protected against homologous parasite challenge. However, some mice developed late, low-level breakthrough parasitaemias. In Chapter 4, the characterisation of two such breakthrough parasitaemias is described. The ama1 genes of the breakthrough parasites were found to be identical to the ama1 gene of the parental parasites. Similarly, no alteration in AMA1 expression was observed. However, the breakthrough parasites were found to be more resistant than the parental parasites to the effects of passive immunisation with rabbit antisera to AMA1, RAP1 and possibly also MSP119. P. chabaudi infections in mice have been previously shown to consist of a primary parasitaemia followed by a short period of subpatency, and a recrudescent parasitaemia. In surface immunofluorescence studies with P. c. chabaudi, parasites of the recrudescence were shown to be distinct from parasites of the primary parasitaemia, with respect to antigens expressed on the surface of late trophozoite- and schizont-infected erythrocytes.
Chapter 4 describes similar surface immunofluorescence assays carried out with P. c. adami infected erythrocytes, and quantitation of fluorescence by flow cytometry. As with P. c. chabaudi, the recrudescent parasites were found to be antigenically distinct from the primary parasitaemia, indicating that antigenic variation had taken place. Because breakthrough parasites from the AMA1 vaccination trial were similar to recrudescences in peak and duration, we hypothesised that breakthrough parasitaemias, like recrudescent parasitaemias, occur as a result of antigenic variation. In Chapter 4 it was shown by surface immunofluorescence and flow cytometry using hyperimmune sera raised against different parasite populations, that breakthrough parasites express antigens on the surface of late trophozoite- and schizont infected erythrocytes that differ from those expressed by the parental and recrudescent parasites. These results support the hypothesis that switching of the variant antigen on the infected erythrocyte surface enables parasites to evade protective antibody responses directed against merozoite antigens.
Chapter 5 describes the cloning and characterisation of P. c. adami RAP1 which was identified in the process of the genomic survey described in Chapter 3, as well as P. berghei RAP1. Both rodent parasite orthologues of RAP1 were found to have 30% sequence similarity to P. falciparum RAP1, and 6 of 8 cysteines were conserved in the rodent parasite orthologues. However the three polypeptides vary significantly in size. P. c. adami RAP1 and P. berghei RAP1 consist of 691 aa and 604 aa respectively, whereas P. falciparum RAP1 consists of 783 aa residues. These size differences reflect very different N-terminal sequences prior to the first cysteine, whereas the cysteine-rich C-terminal regions are more conserved. Both P. falciparum RAP1 and P. c. adami RAP1 contain N-terminal repeats, however they bear no sequence similarity to each other. P. berghei RAP1 lacks N-terminal sequence repeats that are characteristic of P. falciparum and P. c. adami RAP1. The large cysteine-rich C-terminal region P. c. adami RAP1 (PcRAP1 C3) was expressed in E. coli as a hexa-his fusion protein. Rabbit antiserum to recombinant PcRAP1 C3 was used to characterise the expression and sub-cellular localisation of the RAP1 antigen. P. c. adami RAP1 was found to have a Mr of approximately 80,000 and was shown by immunofluorescence to localise to the merozoite rhoptries. Passive immunisation of mice with rabbit anti-RAP1 serum was shown to protect against fulminant parasitaemia and mortality. In a mouse vaccination trial using the recombinant PcRAP1 C3 polypeptide partial protection was conferred against homologous parasite challenge.
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Taylor, Jesse Earl. "Host structuring of parasite populations: Some theoretical and computational studies." Diss., The University of Arizona, 2003. http://hdl.handle.net/10150/289991.
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Because the ecological and the genetic interactions occurring between parasites belonging to different infections are constrained by the physical discreteness of the hosts, the host-parasite association imparts a spatial structure to the populations of parasitic microorganisms. Equating infections with demes or islands, the parasite population can be described by a variant of Wright's island model, in which recovery and infection correspond to extinction and colonization and superinfection corresponds to migration. Here we investigate some of the population genetic consequences of host structure using a combination of theoretical and computational methods. In our first study, we introduce a measure-valued process as a model for the evolution of an age-structured parasite metapopulation and show how to approximate this process using the measure flow generated by a jump-diffusion. We characterize the invariant measures and corresponding jump distributions for the approximation and apply these methods to an example involving a single locus subject to mutation, selection, and genetic drift within hosts and to bottlenecks and bias during transmission. When intrahost selection and transmission bias act discordantly, it is shown that the invariant measure and the jump distribution can differ substantially. We discuss the implications of such discordance for vaccine target selection and review the evidence for biased transmission of HIV-1. In our second study, we use a branching Fisher-Wright process to characterize diversity in an exponentially expanding epidemic. We derive a renewal equation for the persistence probability of the branching diffusion and show that with sufficiently rapid branching a set of k neutral alleles can persist indefinitely with positive probability. In the last study, we exploit the relationship between population recombination rates and superinfection rates to quantify intra-subtype superinfection by HIV-1 in populations from Africa, China, Thailand, Trinidad and Tobago, and the US. Comparison of the population recombination rates estimated for these data sets with those found for data sets simulated using a structured coalescent process representing HIV-1 evolution within an epidemiologically closed population indicates that per-sequence superinfection rates are probably not less than 15% of the corresponding infection rates.
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Diaz, Yacobazzo Alvaro Juan. "A search for mechanism restricting activation of the host complement system in Echinococcus granulosus." Thesis, University of Oxford, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.361948.
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Dehlawi, M. S. "Mast cell responses to intestinal nematodes in mice." Thesis, University of Nottingham, 1986. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.376170.
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De, Aguiar J. C. S. "Studies on the polymorphic schizont antigen of Plasmodium chabaudi." Thesis, Open University, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.383640.
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Ahmed, Rubina. "Elucidation of the role of mannose binding lectin and ST2 in the immune response to the parasitic helminth Brugia malayi." Thesis, Royal Veterinary College (University of London), 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.559018.
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