Relevant bibliographies by topics / Parasites – Immunologie

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  2. Dissertations / Theses
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Academic literature on the topic 'Parasites – Immunologie'

Author: Grafiati
Published: 4 June 2021
Last updated: 15 February 2022

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Journal articles on the topic "Parasites – Immunologie"

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Greenwood, B. M. "Parasite Immunology and the clinical immunologist." Parasite Immunology 23, no. 10 (October 2001): 517. http://dx.doi.org/10.1046/j.1365-3024.2001.00413.x.

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POULIN, R. "Relative infection levels and taxonomic distances among the host species used by a parasite: insights into parasite specialization." Parasitology 130, no. 1 (December 13, 2004): 109–15. http://dx.doi.org/10.1017/s0031182004006304.

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Parasites often exploit more than one host species at any stage in their life-cycle, but the extent to which these host species are used varies greatly. Parasites typically achieve their highest prevalence, intensity and/or abundance in one host species (the principal host), whereas infection levels in auxiliary hosts range from relatively high to very low. The present study examines what influences the distribution of parasite individuals among their different host species, using metazoan parasites that use freshwater fish as their definitive or only host. Specifically, I test the hypothesis that differences in relative infection levels by a parasite among its auxiliary hosts are proportional to the taxonomic distance between the respective auxiliary hosts and the parasite's principal host. Taxonomic distance among hosts is a surrogate measure of their similarity in terms of ecology, physiology and immunology. Using data on 29 parasite species and 6 fish communities, for a total of 47 parasite-locality combinations, it was found that taxonomic distance between the auxiliary hosts and the principal host had no real influence on infection levels in auxiliary hosts, measured as either prevalence, intensity or abundance. The analysis revealed differences in the degree of specialization among major groups of parasites: in terms of abundance or intensity, auxiliary hosts were less important for cestodes than for nematodes and copepods. The lack of an effect of taxonomic distance may indicate that ecological similarity among host species, arising from convergence and not from relatedness, is more important than host phylogeny or taxonomy. Although the results are based on a limited number of parasite taxa, they suggest that parasites may be opportunistic in their colonization of new hosts, and not severely constrained by evolutionary baggage.
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Kim, Ju Yeong, Myung-Hee Yi, and Tai-Soon Yong. "Allergen-like Molecules from Parasites." Current Protein & Peptide Science 21, no. 2 (March 10, 2020): 186–202. http://dx.doi.org/10.2174/1389203720666190708154300.

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Parasite infections modulate immunologic responses, and the loss of parasite infections in the last two to three decades might explain the increased prevalence of allergic diseases in developed countries. However, parasites can enhance allergic responses. Parasites contain or release allergen-like molecules that induce the specific immunoglobulin, IgE, and trigger type-2 immune responses. Some parasites and their proteins, such as Anisakis and Echinococcus granulosus allergens, act as typical allergens. A number of IgE-binding proteins of various helminthic parasites are cross-reactive to other environmental allergens, which cause allergic symptoms or hamper accurate diagnosis of allergic diseases. The cross-reactivity is based on the fact that parasite proteins are structurally homologous to common environmental allergens. In addition, IgE-binding proteins of parasites might be useful for developing vaccines to prevent host re-infection. This review discusses the functions of the IgE-biding proteins of parasites.
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Duneau, David, and Dieter Ebert. "The role of moulting in parasite defence." Proceedings of the Royal Society B: Biological Sciences 279, no. 1740 (April 11, 2012): 3049–54. http://dx.doi.org/10.1098/rspb.2012.0407.

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Parasitic infections consist of a succession of steps during which hosts and parasites interact in specific manners. At each step, hosts can use diverse defence mechanisms to counteract the parasite's attempts to invade and exploit them. Of these steps, the penetration of parasites into the host is a key step for a successful infection and the epithelium is the first line of host defence. The shedding of this protective layer (moulting) is a crucial feature in the life cycle of several invertebrate and vertebrate taxa, and is generally considered to make hosts vulnerable to parasites and predators. Here, we used the crustacean Daphnia magna to test whether moulting influences the likelihood of infection by the castrating bacterium Pasteuria ramosa . This parasite is known to attach to the host cuticula before penetrating into its body. We found that the likelihood of successful parasite infection is greatly reduced if the host moults within 12 h after parasite exposure. Thus, moulting is beneficial for the host being exposed to this parasite. We further show that exposure to the parasite does not induce hosts to moult earlier. We discuss the implications of our findings for host and parasite evolution and epidemiology.
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McRobert, Louisa, Peter Preiser, Sarah Sharp, William Jarra, Mallika Kaviratne, Martin C. Taylor, Laurent Renia, and Colin J. Sutherland. "Distinct Trafficking and Localization of STEVOR Proteins in Three Stages of the Plasmodium falciparum Life Cycle." Infection and Immunity 72, no. 11 (November 2004): 6597–602. http://dx.doi.org/10.1128/iai.72.11.6597-6602.2004.

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ABSTRACT The genome of Plasmodium falciparum harbors three extensive multigene families, var, rif, and stevor (for subtelomeric variable open reading frame), located mainly in the subtelomeric regions of the parasite's 14 chromosomes. STEVOR variants are known to be expressed in asexual parasites, but no function has as yet been ascribed to this protein family. We have examined the expression of STEVOR proteins in intraerythrocytic sexual stages, gametocytes, and extracellular sporozoites isolated from infected Anopheles mosquitoes. In gametocytes, stevor transcripts appear transiently early in development but STEVOR proteins persist for several days and are transported out of the parasite, travel through the host cell cytoplasm, and localize to the erythrocyte plasma membrane. In contrast to asexual parasites, gametocytes move STEVOR to the periphery via a trafficking pathway independent of Maurer's clefts. In sporozoites, STEVOR appear dispersed throughout the cytoplasm in vesicle-like structures. The pattern of STEVOR localization we have observed in gametocytes and sporozoites differs significantly from that in asexual parasite stages. STEVOR variants are therefore likely to perform different functions in each stage of the parasites life cycle in which they occur.
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KOEHLER, ANSON V., and ROBERT POULIN. "Clone-specific immune reactions in a trematode-crustacean system." Parasitology 139, no. 1 (October 14, 2011): 128–36. http://dx.doi.org/10.1017/s0031182011001739.

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SUMMARYVariability of immune responses is an essential aspect of ecological immunology, yet how much of this variability is due to differences among parasite genotypes remains unknown. Here, variation in immune response of the crab, Macrophthalmus hirtipes, is examined as a function of experimental exposure to 10 clonal cercarial lineages of the trematode Maritrema novaezealandensis. Our goals were (1) to assess the variability of the host immune reaction elicited by 10 parasite clones, (2) to test if the heterozygosity–fitness correlation, whereby organisms with higher heterozygosities achieve a higher fitness than those with lower heterozygosities, applies to heterozygous parasites eliciting weak immune responses, and (3) to see how concomitant infections by other macroparasites influence the crab's immune response to cercariae. Parasite clones were distinguished and heterozygosities calculated using 20 microsatellite markers. We found that exposure to cercariae resulted in increased haemocyte counts, and that although interclonal differences in immune response elicited were detected, parasite heterozygosity did not correlate with host immune response. Additionally, the presence of other pre-existing parasites in hosts did not influence their immune response following experimental exposure to cercariae. Overall, the existence of variability in immune response elicited by different parasite clones is promising for future ecological immunology studies using this system.
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Hofmeester, Tim R., Esther J. Bügel, Bob Hendrikx, Miriam Maas, Frits F. J. Franssen, Hein Sprong, and Kevin D. Matson. "Parasite Load and Site-Specific Parasite Pressure as Determinants of Immune Indices in Two Sympatric Rodent Species." Animals 9, no. 12 (November 22, 2019): 1015. http://dx.doi.org/10.3390/ani9121015.

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Wildlife is exposed to parasites from the environment. This parasite pressure, which differs among areas, likely shapes the immunological strategies of animals. Individuals differ in the number of parasites they encounter and host, and this parasite load also influences the immune system. The relative impact of parasite pressure vs. parasite load on different host species, particularly those implicated as important reservoirs of zoonotic pathogens, is poorly understood. We captured bank voles (Myodes glareolus) and wood mice (Apodemus sylvaticus) at four sites in the Netherlands. We sampled sub-adult males to quantify their immune function, infestation load for ecto- and gastrointestinal parasites, and infection status for vector-borne microparasites. We then used regression trees to test if variation in immune indices could be explained by among-site differences (parasite pressure), among-individual differences in infestation intensity and infection status (parasite load), or other intrinsic factors. Regression trees revealed splits among sites for haptoglobin, hemagglutination, and body-mass corrected spleen size. We also found splits based on infection/infestation for haptoglobin, hemolysis, and neutrophil to lymphocyte ratio. Furthermore, we found a split between species for hemolysis and splits based on body mass for haptoglobin, hemagglutination, hematocrit, and body-mass corrected spleen size. Our results suggest that both parasite pressure and parasite load influence the immune system of wild rodents. Additional studies linking disease ecology and ecological immunology are needed to understand better the complexities of host–parasite interactions and how these interactions shape zoonotic disease risk.
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Chen, Xian-Ming, Steven P. O'Hara, Bing Q. Huang, Jeremy B. Nelson, Jim Jung-Ching Lin, Guan Zhu, Honorine D. Ward, and Nicholas F. LaRusso. "Apical Organelle Discharge by Cryptosporidium parvum Is Temperature, Cytoskeleton, and Intracellular Calcium Dependent and Required for Host Cell Invasion." Infection and Immunity 72, no. 12 (December 2004): 6806–16. http://dx.doi.org/10.1128/iai.72.12.6806-6816.2004.

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ABSTRACT The apical organelles in apicomplexan parasites are characteristic secretory vesicles containing complex mixtures of molecules. While apical organelle discharge has been demonstrated to be involved in the cellular invasion of some apicomplexan parasites, including Toxoplasma gondii and Plasmodium spp., the mechanisms of apical organelle discharge by Cryptosporidium parvum sporozoites and its role in host cell invasion are unclear. Here we show that the discharge of C. parvum apical organelles occurs in a temperature-dependent fashion. The inhibition of parasite actin and tubulin polymerization by cytochalasin D and colchicines, respectively, inhibited parasite apical organelle discharge. Chelation of the parasite's intracellular calcium also inhibited apical organelle discharge, and this process was partially reversed by raising the intracellular calcium concentration by use of the ionophore A23187. The inhibition of parasite cytoskeleton polymerization by cytochalasin D and colchicine and the depletion of intracellular calcium also decreased the gliding motility of C. parvum sporozoites. Importantly, the inhibition of apical organelle discharge by C. parvum sporozoites blocked parasite invasion of, but not attachment to, host cells (i.e., cultured human cholangiocytes). Moreover, the translocation of a parasite protein, CP2, to the host cell membrane at the region of the host cell-parasite interface was detected; an antibody to CP2 decreased the C. parvum invasion of cholangiocytes. These data demonstrate that the discharge of C. parvum sporozoite apical organelle contents occurs and that it is temperature, intracellular calcium, and cytoskeleton dependent and required for host cell invasion, confirming that apical organelles play a central role in C. parvum entry into host cells.
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TURNER, A. K., P. M. BELDOMENICO, K. BOWN, S. J. BURTHE, J. A. JACKSON, X. LAMBIN, and M. BEGON. "Host–parasite biology in the real world: the field voles of Kielder." Parasitology 141, no. 8 (March 10, 2014): 997–1017. http://dx.doi.org/10.1017/s0031182014000171.

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SUMMARYResearch on the interactions between the field voles (Microtus agrestis) of Kielder Forest and their natural parasites dates back to the 1930s. These early studies were primarily concerned with understanding how parasites shape the characteristic cyclic population dynamics of their hosts. However, since the early 2000s, research on the Kielder field voles has expanded considerably and the system has now been utilized for the study of host–parasite biology across many levels, including genetics, evolutionary ecology, immunology and epidemiology. The Kielder field voles therefore represent one of the most intensely and broadly studied natural host–parasite systems, bridging theoretical and empirical approaches to better understand the biology of infectious disease in the real world. This article synthesizes the body of work published on this system and summarizes some important insights and general messages provided by the integrated and multidisciplinary study of host–parasite interactions in the natural environment.
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Persson, Catrine M., Henrik Lambert, Polya P. Vutova, Isabel Dellacasa-Lindberg, Joanna Nederby, Hideo Yagita, Hans-Gustaf Ljunggren, Alf Grandien, Antonio Barragan, and Benedict J. Chambers. "Transmission of Toxoplasma gondii from Infected Dendritic Cells to Natural Killer Cells." Infection and Immunity 77, no. 3 (January 12, 2009): 970–76. http://dx.doi.org/10.1128/iai.00833-08.

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ABSTRACT The obligate intracellular parasite Toxoplasma gondii can actively infect any nucleated cell type, including cells from the immune system. In the present study, we observed that a large number of natural killer (NK) cells were infected by T. gondii early after intraperitoneal inoculation of parasites into C57BL/6 mice. Interestingly, one mechanism of NK cell infection involved NK cell-mediated targeting of infected dendritic cells (DC). Perforin-dependent killing of infected DC led to active egress of infectious parasites that rapidly infected adjacent effector NK cells. Infected NK cells were not efficiently targeted by other NK cells. These results suggest that rapid transfer of T. gondii from infected DC to effector NK cells may contribute to the parasite's sequestration and shielding from immune recognition shortly after infection.
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Dissertations / Theses on the topic "Parasites – Immunologie"

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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
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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
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Books on the topic "Parasites – Immunologie"

1

Wakelin, Derek. Immunity to parasites: How parasitic infections are controlled. 2nd ed. Cambridge: Cambridge University Press, 1996.

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Leopoldina-Meeting Parasitismus, Immunreaktionen bei Parasitosen (1991 Halle an der Saale, Germany). Leopoldina-Meeting Parasitismus, Immunreaktionen bei Parasitosen: Vom 25. bis 26. Oktober 1991 in Halle (Saale). Halle, Saale: Deutsche Akademie der Naturforscher Leopoldina, 1992.

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Kennedy, M. W., and W. Harnett, eds. Parasitic nematodes: molecular biology, biochemistry and immunology. Wallingford: CABI, 2013. http://dx.doi.org/10.1079/9781845937591.0000.

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Kennedy, M. W., and W. Harnett, eds. Parasitic nematodes: molecular biology, biochemistry and immunology. Wallingford: CABI, 2001. http://dx.doi.org/10.1079/9780851994239.0000.

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Maule, A. G., and N. J. Marks, eds. Parasitic flatworms: molecular biology, biochemistry, immunology and physiology. Wallingford: CABI, 2005. http://dx.doi.org/10.1079/9780851990279.0000.

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Immunity to parasitic infections. Chichester, West Sussex, UK: John Wiley & Sons, 2012.

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Evolutionary parasitology: The integrated study of infections, immunology, ecology, and genetics. Oxford: Oxford University Press, 2011.

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Kreier, Julius P. Infection, resistance and immunity. 2nd ed. New York, NY: Taylor & Francis, c2002., 2002.

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Kreier, Julius P. Infection, resistance and immunity. 2nd ed. New York, NY: Taylor & Francis, c2002., 2002.

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F, Mortensen Richard, ed. Infection, resistance, and immunity. New York: Harper & Row, 1990.

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Book chapters on the topic "Parasites – Immunologie"

1

Maruyama, Haruhiko, and Yukifumi Nawa. "Immunology of the Infection." In World Class Parasites, 337–81. Boston, MA: Springer US, 2007. http://dx.doi.org/10.1007/978-0-387-71358-8_10.

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Hadley, Terence J., and Louis H. Miller. "Invasion of Erythrocytes by Malaria Parasites: Erythrocyte Ligands and Parasite Receptors." In Chemical Immunology and Allergy, 49–71. Basel: KARGER, 1988. http://dx.doi.org/10.1159/000318613.

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Hu, Guoku, Yaoyu Feng, Steven P. O’Hara, and Xian-Ming Chen. "Immunology of Cryptosporidiosis." In Cryptosporidium: parasite and disease, 423–54. Vienna: Springer Vienna, 2013. http://dx.doi.org/10.1007/978-3-7091-1562-6_10.

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Kaye, Paul M. "The Immunology of Visceral Leishmaniasis: Current Status." In World Class Parasites, 137–50. Boston, MA: Springer US, 2002. http://dx.doi.org/10.1007/978-1-4615-0955-4_10.

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Owen, Jeb P., and Dana M. Hawley. "Host-Parasite Interactions." In Eco-immunology, 73–92. Dordrecht: Springer Netherlands, 2014. http://dx.doi.org/10.1007/978-94-017-8712-3_4.

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Black, Samuel J., and Cynthia L. Baldwin. "Impact assessment of immunology and immunoparasitology research at ILRAD and ILRI." In The impact of the International Livestock Research Institute, 164–207. Wallingford: CABI, 2020. http://dx.doi.org/10.1079/9781789241853.0164.

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Abstract This book chapter assesses the research on bovine immunology and immunoparasitology conducted over 42 years, from 1973 to 2015, first at ILRAD (1973-1994) and subsequently at ILRI, which was formed by merging ILRAD and the International Livestock Centre for Africa (ILCA) in 1995. This assessment covers the approaches taken, the performance of research teams, the scientific truths uncovered, the cost-effectiveness of the research undertaken and the practical outcomes achieved, notably, the development of monoclonal antibodies (mAbs) and other tools to better define the bovine immune system. The chapter makes extensive use of citation data along with the personal reflections of scientists who participated in the research and surveys of opinion leaders in the field. The specific scientific goals and achievements of ILRI and its predecessors were as follows: making a substantive contribution to bovine immunology was realistic and has been substantially achieved, measuring the diversity of strains of Theileria parva, Trypanosoma brucei, Trypanosoma vivax and Trypanosoma congolense was realistic and has been substantially achieved, identifying mechanisms of immunity that kill parasites or limit the growth of the above parasites was realistic and has been substantially achieved, and developing an effective subunit vaccine against any of the parasites was an ambitious goal and so far has not been achieved.
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Farrell, Jay P. "The Immunology of Cutaneous Leishmaniasis: Experimental Infections and Human Disease." In World Class Parasites, 151–68. Boston, MA: Springer US, 2002. http://dx.doi.org/10.1007/978-1-4615-0955-4_11.

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Ackers, J. P. "Immunologic Aspects of Human Trichomoniasis." In Trichomonads Parasitic in Humans, 36–52. New York, NY: Springer New York, 1990. http://dx.doi.org/10.1007/978-1-4612-3224-7_4.

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Mansfield, John M., and Martin Olivier. "Immune Evasion by Parasites." In Immunology of Infectious Diseases, 379–92. Washington, DC, USA: ASM Press, 2014. http://dx.doi.org/10.1128/9781555817978.ch25.

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Sam-Yellowe, Tobili Y. "Parasite Immunity." In Immunology: Overview and Laboratory Manual, 145–49. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-64686-8_19.

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