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Dissertations / Theses on the topic 'Immunology and Allergy'
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1
Sjögren, Ylva. "Early infant gut flora and neutral oligosaccharides in colostrum in relation to allergy development in children." Licentiate thesis, Stockholm University, Wenner-Gren Institute for Experimental Biology, 2007. http://urn.kb.se/resolve?urn=urn:nbn:se:su:diva-7152.
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<p>Today, atopic allergy is the most common chronic disease among children in the developed world. The increase in allergy prevalence during the past decades in these countries might be associated with lower microbial exposure. The gut flora, consisting of approximately 800 different species of bacteria, has been postulated to be important for the development of a fully functional immune system. Essentially, these bacteria are in constant contact with the gut flora associated lymphoid tissue, the largest lymphoid tissue of the human body. Following birth, the sterile gut of the newborn is immediately colonised by various bacterial species. Actually, alterations in the infant gut flora have been associated with allergy development.</p><p>Human milk is the major food in infancy and could thus influence the composition of the infant gut flora. Immunomodulatory components in human milk might differ between mothers and could therefore explain the contradictory results seen regarding breastfeeding and allergy development. Oligosaccharides, the third most abundant solid component in human milk, survive the passage through the stomach and are utilised by the gut microbiota. We analysed nine abundant neutral oligosaccharides in colostrum samples from allergic and non-allergic women and related to subsequent allergy development in their children. We found a considerable variation in the concentration of neutral oligosaccharides in colostrum, which was not to be explained by the allergic status of the women. Neither was the consumption of neutral colostrum oligosaccharides related to the allergy development in children.</p><p>Relevant bacterial species in early faecal samples were analysed, with Real-time PCR, and related to allergy development in children followed up to five years of age. Infants who harboured Lactobacilli (L.) group I (L. rhamnosus, L. paracasei, L. casei) at 1 week of age and Bifidobacterium adolescentis at 1 month of age developed allergic disease less frequently during their first five years than infants who did not harbour these bacteria at the same time (p=0.004 and p=0.008 respectively).</p><p>In conclusion, the work presented in this thesis implies the importance of a diverse gut flora early in life for the development of a fully functional immune system. However, consumption of colostrum with high amounts of neutral oligosaccharides does not protect against early allergy development.</p>
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Kronqvist, Marianne. "Clinical and immunological studies of respiratory allergy among farmers : with focus on dust mite allergy /." Stockholm, 2000. http://diss.kib.ki.se/2000/91-628-4411-3/.
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Thang, Cin. "Investigation of intervention strategies for Ig-E mediated food allergy in a murine model of cow's milk allergy." Thesis, McGill University, 2013. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=119562.
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Food allergy, an immune-mediated adverse hypersensitivity reaction to ingested food, is an emerging global health problem that not only causes the disease to susceptible individuals but also causes psychological impacts and financial damage to their families. Food allergy incidence is significantly increased in the past decade and currently estimated at 6-8% in 1 year old children, and 2-4% in older children and adults. Food allergy is the leading cause of anaphylaxis in children and severe cases may lead to fatal anaphylaxis reactions. Although continuous efforts have been made to better understand the nature of allergens, predisposing environmental factors, and the host's immune response mechanisms, there is no cure available for food allergy today. In this study, we have investigated three food allergy reducing strategies by supplementing probiotics, low doses of allergens and omega-3 poly unsaturated fatty acids (ω-3 PUFAs) in cow's milk protein sensitized Balb/c mice. Lactobacillus rhamnosus GG (LGG) supplementation had tendency to promote Th1 response while VSL#3 provided more potent allergy reducing effects via inducing intestinal secretory IgA (sIgA). Low doses of allergen administration offered suppression of allergen-specific immune responses via Treg-mediated active suppression, indicated by suppressing both allergen-specific Th1 response [reduced BLG-specific serum IgG2a and elevated IL-12(p40)], and Th2 response [lower BLG-specific serum IgE and IgG]. Interestingly, mice received both VSL#3 and low doses of allergen exhibited both allergen-specific active suppression effects and higher sIgA production. We then investigated the effects of different levels of ω-3 and ω-6 PUFAs in the energy and fat rich Western-style diet on food allergy development. Observation of elevated BLG-specific serum immunoglobulins in all experimental mice indicated that both ω-3 and ω-6 PUFAs failed to prevent the development of allergen-specific immune response. However, ω-3 PUFAs alleviated anaphylactic reactions and the severity of allergic reaction as indicated by the unchanged rectal temperature, lower hypersensitivity scores, and Th1-favoured immune responses in BLG-sensitized O3H mice. In general, this study revealed the promising strategies for treatments and prevention against food allergy in the near future.<br>Les allergies alimentaires, réactions dues à une hypersensibilité du système immunitaire après ingestion d'un certain type d'aliments, constituent un problème de santé publique croissant qui, en plus de dégrader la santé des individus susceptibles, engendre un impact psychologique et financier pour les familles touchées. L'incidence des allergies alimentaires a significativement augmenté ces dernières années et le taux est actuellement estimé être de 6-8% chez les jeunes enfants d'1 an et de 2-4% chez les autres enfants et les adultes. Les allergies alimentaires représentent la première cause d'anaphylaxie chez l'enfant et plusieurs cas d'allergies peuvent causer une réaction anaphylactique fatale. Bien que des efforts continus aient été faits pour tenter de mieux comprendre la nature des allergènes, les facteurs environnementaux prédisposant aux allergies et les mécanismes de la réponse immunitaire, aucun traitement contre les allergies alimentaires n'est disponible à l'heure actuelle. Dans cette étude, nous avons testé trois différentes stratégies visant à réduire l'allergie alimentaire, à savoir l'utilisation de probiotiques, de faibles doses d'allergènes et d'acides gras polyinsaturés oméga-3 chez des souris Balb/c sensibilisées aux protéines de lait de vache. L'administration de Lactobacillus rhamnosus GG (LGG) a montré une tendance à promouvoir une activation des cellules Th1 alors que VSL#3 a engendré une plus forte réduction de l'allergie via l'induction de la sécrétion intestinale d'IgA (sIgA). L'administration de faibles doses d'allergènes a provoqué une suppression de la réponse immunitaire dirigée contre les allergènes via l'activation des cellules Treg, ceci étant suggéré par la suppression des réponses immunitaires Th1 spécifique [diminution des IgG2a BLG-spécifiques et augmentation des IL-12(p40)] et Th2 spécifique [diminution des IgE et IgG BLG-spécifiques]. De plus, les souris ayant reçu à la fois VSL#3 et des faibles doses d'allergènes ont montré une suppression des effets de la réponse allergénique et une production plus élevée de sIgA. Nous avons ensuite étudié les effets de différents niveaux d'oméga-3 et d'oméga-6 dans un régime alimentaire de type occidental riche en énergie et en matières grasses sur le développement des allergies alimentaires. L'observation d'une élévation des immunoglobulines BLG-spécifiques chez toutes les souris expérimentales ont indiqué que les oméga-3 et -6 n'ont pas réussi à empêcher le développement de la réponse immunitaire dirigée contre les allergènes. Cependant, les oméga-3 ont diminué les réactions anaphylactiques et le degré de sévérité de la réaction allergique, ceci étant suggéré par un score d'hypersensibilité plus faible, une absence de changement de la température rectale et une réponse immunitaire favorisée par les cellules Th1. Pour conclure, cette étude a révélé des stratégies prometteuses pour le traitement et la prévention des allergies alimentaires dans les années à venir.
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Minang, Jacob. "Cytokine responses in metal-induced allergic contact dermatitis : Relationship to in vivo responses and implication for in vitro diagnosis." Doctoral thesis, Stockholm : Dept. of Immunology, Wenner-Gren Institute, Stockholm University, 2005. http://urn.kb.se/resolve?urn=urn:nbn:se:su:diva-717.
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Klaesson, Sven. "Immune modulatory effects of intravenous immunoglobulin in vitro and after allogeneic bone marrow transplantation /." Stockholm, 1997. http://diss.kib.ki.se/1997/91-628-2636-0.
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Barbieri, Bruno. "Novel aspects of p-aminobenzoic acid metabolism in connection with arachidonic acid oxidation in human lymphoid cells and platelets /." Stockholm, 1997. http://diss.kib.ki.se/1997/91-628-2679-4.
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Larsson, Susanne. "Human cytomegalovirus (HCMV) : detection and elimination of infected blood cells in vitro, immune reactivity and complications following HCMV infection /." Stockholm, 1998. http://diss.kib.ki.se/1998/91-628-2883-5.
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Kumagai-Braesch, Makiko. "Immunological characterisation of human anti-pig responses in vitro /." Stockholm, 1998. http://diss.kib.ki.se/1998/91-628-2959-9.
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Hammarström, Viera. "B-cell immunity in patients with hematological malignancies and after stem cell transplantation : studies with special reference to tetanus and pneumococcal immunity /." Stockholm, 1998. http://diss.kib.ki.se/search/diss.se.cfm?19980828hamm.
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Zetterquist, Henrik. "The use of molecular techniques for identification of genetic divergence in transplantation : with special reference to MHC genes and HLA typing /." Stockholm, 1998. http://diss.kib.ki.se/1998/91-628-3267-0/.
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Huang, DeRen. "Genetic control of myasthenia gravis : a study on cytokine and co-stimulator genes and their related functions /." Stockholm, 1999. http://diss.kib.ki.se/1999/91-628-3478-9/.
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Elkarim, Rihab A. "Potential role of anti-cytokine autoantibodies in the regulation of cytokine responses in infections and autoimmune diseases /." Stockholm, 1999. http://diss.kib.ki.se/1999/91-628-3774-5/.
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Gough, Lucy. "The proteolytic activity of the mite allergen Der p 1 enhances IgE synthesis : studies in mice showing a link between allergenicity and cysteine protease activity." Thesis, University of Nottingham, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.342508.
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Boyd, Peter. "Hapten-mediated contact allergy : a proteomic and immunological approach." Thesis, University of Southampton, 2014. https://eprints.soton.ac.uk/369220/.
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Allergic contact dermatitis (ACD) is a prevalent skin condition caused by chemical haptens, which enter the epidermis, and by modifying self-proteins, render them immunogenic via the activation of hapten-specific T-cells. It is currently not known which specific protein modifications are responsible for sensitization. This work investigates the extreme sensitizer DNCB, which confers a dinitrophenyl (DNP) protein modification. Immortalised keratinocytes (HaCaT), incubated with DNCB were compared to ex vivo human skin using immunofluorescence and western blot detection of DNP-proteins, showing widespread protein modification and similarities between tissue and cells when using a clinical dose. Proliferation assays using lymphocytes from DNCB-sensitive donors showed responses to DNP proteins isolated from DNCB-treated HaCaT cells and primary keratinocytes. While western blot analysis of pH gradient separated fractions identified a number of DNP-proteins in the DNP-HaCaT cell lysates, these were not immunogenic in lymphocyte assays. The model protein human serum albumin (HSA) was used to investigate the modification kinetics of DNCB by identifying which amino acid residues were changed more readily using a range of DNCB concentrations and incubation times. Cysteine residues, including those in disulphide bonds and particularly cysteine 34 are more readily modified than lysine in HSA, suggesting that DNCB is able to alter the structure of proteins. A novel process of hapten-reversal by a process termed ‘thiolysis’ was found to remove DNP groups from the cysteine residues of synthetic peptides derived from the sequence of HSA containing cysteine 34 using the reducing agent dithiothreitol. Identical peptides with C34>K34 showed no such hapten-reversal. This corresponds to the unexpected immunogenicity of the cysteinyl peptide and also the DNP modified tripeptide glutathione. Anti-DNP western blots show that the DNP group is transferred to other proteins during incubation with human monocytes in culture. This suggests a cellular process of removing DNP groups and GILT, a thiol reductase present in the endosomes is presented as a candidate for this process. This work demonstrates that DNCB can generate a wide variety of DNP protein adducts and that cysteinyl moieties are able to stimulate lymphocyte proliferation by way of hapten transfer. This highlights a potentially novel process involved in the mechanism of contact allergy.
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Musaad, Salma MA. "Anthropometric Measures of Obesity and the Association with Asthma and Other Allergic Disorders: Cincinnati Children’s Allergy and Immunology Clinic Cohort." University of Cincinnati / OhioLINK, 2007. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1192570691.
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See, Sarah Bihui. "Outer membrane protein immunity to Pasteurella pneumotropica and the interaction of allergy." University of Western Australia. School of Paediatrics and Child Health, 2010. http://theses.library.uwa.edu.au/adt-WU2010.0103.
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[Truncated abstract] Infectious and allergic diseases of the respiratory tract are major contributors to global mortality, morbidity and economic burden. Bacterial infections such as pneumonia and otitis media are important diseases, especially in children, while allergic diseases such as asthma and allergic rhinitis afflict up to 30% of the world's population. A confounding aspect of respiratory disease is the evidence of a complex relationship between respiratory allergy and respiratory infection, with infection suggested to both promote and prevent the pathogenesis of allergic disease. Additionally, allergy is a risk factor for bacterial infection such as otitis media, pneumonia and sinusitis, while respiratory infection can exacerbate allergic symptoms. Given the burden of bacterial respiratory disease and respiratory allergy, the development of preventative treatments for these diseases is needed and will benefit from clearer knowledge of the underlying immune mechanisms. This thesis aimed to to extend current knowledge by using Pasteurella pneumotropica, a similar bacteria to the human pathogen nontypeable Haemophilus influenzae (NTHi), to study respiratory infection and protective anti-outer membrane protein (OMP) immunity as well as the interaction of respiratory infection and allergic inflammation. Homologues of the important NTHi vaccine candidates P4, P6, P26 and D15 were found to be encoded by P. pneumotropica and a high level of amino acid sequence identity was noted between the different P. pneumotropica strains, as well as between other Pasteurellaceae members. ... In contrast, anti-P6his serum antibodies transferred to naïve mice did not confer protection. These results suggested that T-cellmediated mechanisms were involved in P6his-mediated protection, and showed that the P. pneumotropcia model was useful for elucidating protective mechansims. The interaction of P. pneumotropica infection and papain-induced allergy was studied to investigate immune mechanisms underlying respiratory infection and allergy. Mice with ongoing allergic inflammation were intranasally challenged with bacteria and exhibited reduced pulmonary bacterial numbers, prolonged eosinophilia in the lungs and the induction of Th2 cytokines in the BALF, compared to nonallergic, infected mice. This suggested a protective role for allergic inflammation in this model. The effect of papaininduced inflammation on mice colonised by P. pneumotropica was also examined and allergic inflammation appeared to worsen infection in colonised mice. This suggested that allergic inflammation may also have a role in promoting infection in this model. In conclusion, this thesis explored mechanisms involved in vaccine-mediated immunity and the interaction of respiratory infection and allergy using a P. pneumotropica infection in its natural host. It was shown that intranasally administered recombinant P6 and P4 protected mice from lung infection, which justifies the inclusion of these OMPs as NTHi vaccine candidates. Additionally, it was demonstrated that the interaction of allergy and respiratory infection modulated immune responses. Overall, these results emphasize that a clearer understanding of the complex mechanisms underlying these interactions is required, and may be aided by the development of suitable animal models.
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Lee, Eric Cheuk Kin. "Characterising the clinical phenotype and immunopathophysiology of food protein-induced enterocolitis syndrome in Australian children." Thesis, University of Sydney, 2020. https://hdl.handle.net/2123/24080.
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FPIES is an uncommon food allergic disorder in infants and children. It differs clinically from IgE-mediated food allergy presenting acutely with delayed profuse vomiting, at times with lethargy, pallor, floppiness and diarrhoea. The diagnosis is difficult as it is based on clinical criteria, with no diagnostic test aside from oral food challenge. There is geographic variation in demographic features and the immunopathophysiology of FPIES is largely unknown. In this thesis, a retrospective study was undertaken to characterise the demographic and clinical phenotype of FPIES in Australian children. Prospective epidemiological and mechanistic studies involving time to resolution, whole blood mRNA profiling and flow cytometric analysis of monocytes and innate lymphoid cells (ILC) were performed to evaluate potential immune mechanisms underpinning FPIES. Here, we demonstrate that rice is the most common food trigger in Australia. Cross-reactivity was commonly seen between rice and oats; and cow’s milk and soy. Children with rice and cow’s milk FPIES achieved resolution at an earlier age compared to those with egg and fish FPIES. Comparison of clinical presentations of children with FPIES, bacterial sepsis or infectious gastroenteritis demonstrated that the absence of fever and normal C-reactive protein was more likely in FPIES. mRNA expression analysis showed upregulation of innate immunity, particularly granulocyte adhesion and triggering receptor expressed on myeloid cells 1 (TREM1) signalling. Flow cytometry demonstrated increased TREM1 expression on classical monocytes in persistent FPIES. Downregulation of B7 integrin in ILC1 was seen, suggesting that ILCs may play a role in regulating tolerance. This data furthers our understanding of FPIES, with a characteristic demographic and clinical profile in Australian children. Although not yet fully understood, preliminary findings suggest that innate immune mechanisms have a key role in the immunopathophysiology of FPIES.
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Cederbrant, Karin. "The primary lymphocyte culture in the diagnosis of drug- and metal-induced allergy /." Linköping : Univ, 2000. http://www.bibl.liu.se/liupubl/disp/disp2000/med635s.pdf.
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Montan, Per. "Immunological and inflammatory mechanisms in ocular allergy with special reference to vernal keratoconjunctivitis : clinical and experimental studies /." Stockholm, 2000. http://diss.kib.ki.se/2000/91-628-4170-X/.
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Järvinen, Kirsi-Marjut. "Human milk immunology in relation to the development of cow's milk allergy in the breast-fed." Helsinki : University of Helsinki, 2000. http://ethesis.helsinki.fi/julkaisut/laa/kliin/vk/jarvinen/.
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Breckler, Liza Anne. "The role of maternal-fetal interactions on the aetiology of allergic disease." University of Western Australia. School of Paediatrics and Child Health, 2009. http://theses.library.uwa.edu.au/adt-WU2010.0042.
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[Truncated abstract] The dramatic increase in the expression of allergic diseases such as asthma and allergy over the last 20-30 years has highlighted the urgent need to identify causative factors. It was hypothesised that direct immune interactions between mother and fetus contribute to the cytokine milieu of pregnancy, thus influencing immune maturation after birth. Further it was speculated that the cytokine responses produced as a result of maternalfetal interactions are Th-2 skewed in women allergic disease, which programmes their offspring towards developing an allergic phenotype after birth. To test this hypothesis a cohort of 169 pregnant women were recruited at 20 weeks gestation and defined as allergic or non-allergic based on both clinical history and skin prick test sensitisation. These women and their infants were followed up throughout pregnancy (20 weeks, 30 weeks, 36 weeks gestation and 6 weeks post-partum) and up to 2.5 years of age. Mixed lymphocyte reactions (MLR) were used to measure maternal cytokine (IL-6, IL-10, IL-13 and IFN-) and lymphoproliferative responses to fetal alloantigens at each pregnancy time-point. Human leukocyte antigen (HLA) typing of mothers and infants were performed to assess the effect of HLA mismatch on maternal MLR responses to their fetus. After delivery, mononuclear cells (MNC) were isolated from cord blood (CB) and stimulated with allergens, mitogen and toll-like receptor (TLR) ligands. .... As IL-6 also participates in adaptive immunity by promoting Th-2 differentiation it is proposed that the production of IL-6 as a results of maternal encounters with paternal antigens during pregnancy, contribute to the Th-2 skewed responses observed universally in most infants at birth. Associations between maternal-fetal interaction and clinical outcomes in infancy: Although clinical signs of allergy in infancy were not the main outcome measure of this thesis, there were interesting, yet complex relationships between the production of these maternal cytokines towards the fetus and allergic disease at infant follow-ups. Increased maternal IFN-¿ to fetal alloantigen was associated with asthma at 2.5 years and a trend towards recurrent wheeze at 12 months. In contrast decreased maternal IL-13 production was associated with IgE mediated food allergy at 12 months. Adjusting for maternal allergy and other potential confounders including infant gender, method of delivery, HLA mismatch, and paternal allergy did not account for these relationships. Further follow-ups of these infants are required to determine if these relationship last in to early childhood. In conclusion, the findings of this thesis provides further support for the hypothesis that immune responses at birth are programmed prenatally, and that this programming has implications later in life. Importantly, the placenta is the immunologically active interface between mother and fetus during pregnancy. Therefore it is emphasised that there is a crucial need for future research to focus on early immune programming at the placental level before the aetiological pathways of immune mediated diseases can be fully elucidated.
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Liang, Juan. "A Nonlinear Mixed Modeling Method to Analyze Allergen Assay Data and the Effects of Exposures Two Indoor Aeroallergens During Infancy on Children at Age Three: The CCAAPS Cohort." Cincinnati, Ohio : University of Cincinnati, 2009. http://rave.ohiolink.edu/etdc/view.cgi?acc_num=ucin1245413088.
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Thesis (Ph.D.)--University of Cincinnati, 2009.<br>Advisor: Paul Succop. Title from electronic thesis title page (viewed Dec. 15, 2009). Keywords: Nonlinear; Immunoassay; Allergen; Allergy. Includes abstract. Includes bibliographical references.
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Azzaoui, Imane. "CCL18 et réponse régulatrice, de la situation physiologique à l'atopie." Thesis, Lille 2, 2011. http://www.theses.fr/2011LIL2S019/document.
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Les chimiokines sont un élément essentiel du trafic cellulaire aussi bien homéostatique que dans des situations pathologiques. Outre cette fonction chimiotactique spécifique à ce type de molécules, on leur a récemment attribué une implication dans le profil de polarisation de la réponse adaptative spécifique, en agissant directement sur les lymphocytes T (Lc T) ou indirectement par le biais des cellules dendritiques (DC). CCL18 est une chimiokine exprimé préférentiellement au niveau pulmonaire et de façon moindre au niveau ganglionnaire, capable d’attirer les DC et les Lc T, elle est induite par les cytokines de type Th2 telle que l'IL-4, l'IL-13, mais aussi par la cytokine immunomodulatrice l'IL-10, son récepteur est inconnu à ce jour. Au laboratoire il a été montré une implication du CCL18 dans l’asthme allergique (de Nadai, JI, 2006), et cette chimiokine a été associée à différentes pathologies à tropisme pulmonaire ou non avec un rôle pas toujours très clair. L'objectif de ce travail a été d’étudier l’effet immunitaire de cette chimiokine, en base et en situation atopique. L'effet direct du CCL18 a été évalué sur la polarisation de la réponse T. Le prétraitement des Lc T mémoire CD4+ CD25-, de sujets non allergiques, avec le CCL18 conduit à leur transformation en Lc T régulateurs CD4+ CD25+ Foxp3+ produisant de l’IL-10 et du TGF-b capables d'inhiber la prolifération des Lc T effecteurs, à la fois par un mécanisme cytokine et contact dépendant. Cependant, cet effet de régulation de CCL18 est perdu lorsque les cellules T proviennent de sujets allergiques (Chang Y et al., FASEB J, 2010). L’effet indirect du CCL18 a été évalué sur la réponse immune via les DC. La différenciation de monocytes de sujets sains en présence de GM-SCF et CCL18 conduit au développement de DC de phénotype semi-mature, expriment le CCR7, produisant de l’IL10 et l’enzyme 2,3-indoleamine dioxigenase et induisant le développent de Lc T régulateurs de type Tr1 produisant de l’IL-10 capables d’inhiber la prolifération de Lc T effecteurs, par un mécanisme cytokine dépendant. Étonnamment, lorsque les monocytes proviennent de patients allergiques, l'effet tolérogène de CCL18 est perdu en liaison avec la diminution de la fixation de CCL18 à son récepteur putatif (Azzaoui I et al., en révision Blood). Par ailleurs, CCL18 pourrait également jouer un rôle dans la résolution de la réaction allergique par un effet chimiotactique vis-à-vis d’une sous population de LcT régulateurs CD4+CD25highCD127lowLAP+ (Chenivesse C et al., en révision JI). L'effet de corticoïdes sur l'expression de CCL18 a ensuite été analysé. Il a été montré que la sécrétion de CCL18 induite par les cytokines IL-4 et IL-10 est potentialisée par la dexaméthasone, ce qui confirme que CCL18 est plutôt une chimiokine à activité anti inflammatoire (Chabrol J et al., en préparation). La dernière étude concerne une approche dans un modèle murin d'asthme allergique, induit par l'ovalbumine chez la souris Balb/cBYJ. D'un point de vue fonctionnel, l'administration de CCL18 recombinant par voie intratrachéale à des animaux sensibilises permet d'inhiber le développement de la réaction asthmatique, en diminuant l'inflammation pulmonaire (réduction de l'infiltration éosinophilique, inhibition de la production locale de cytokines Th2) et protège ces derniers contre l'altération de leur fonction respiratoire (protection contre l'hyperréactivité bronchique, avec inhibition de l'hypersécrétion de mucus). Toutefois, les mécanismes cellulaires à l'origine de cette protection semblent indépendants de grandes voies de régulation de la réaction (Gilet J et al., en préparation). L'ensemble de ces études montre, et pour la première, qu’une chimiokine est capable d’induire le développement d’une réponse tolérogénique<br>Chemokines are a key component of homeostatic cell traffic and involved in pathological situations. In addition to this chemotactic function, specific to these molecules, they have been recently assigned an involvement in specific adaptive response polarization, by acting directly on T cells (T Lc) or indirectly through dendritic cells (DC). CCL18 is a chemokine preferentially expressed in lung and lymph nodes, able to attract DCs and T Lc, induced by Th2 cytokines such as IL-4, IL-13 but also by the immunomodulatory cytokine IL-10, and its receptor is still unknown. In our laboratory it was shown an involvement of CCL18 in allergic asthma (de Nadai, JI, 2006), and this chemokine has also been associated with various pathologies without areal clear described role. The purpose of this work was to evaluate the immune effect of CCL18 at baseline and in atopic situation. The direct effect of CCL18 was evaluated on T cell polarization. Pretreatment of memory T cells CD4+CD25-, from non allergic subjects, with CCL18 led to their switch to regulatory CD4+CD25+ Foxp3+ cells, able to produce IL-10 and TGF-b and inhibit effectors T cell proliferation, by a contact and cytokine dependent mechanism. However, this regulatory effect of CCL18 was lost when T cells were derived from allergic subjects (Chang Y et al., FASEB J, 2010). The indirect effect of CCL18 has been assessed on the immune response through DC. Monocyte, from healthy subjects, differentiated in DC with GM-CFS and CCL18 led to development of semi-mature DC, that expressed CCR7 and produced IL10 and the enzyme indoleamine 2,3-inducing dioxigenase. These cells primed regulatory Tr1 cells able to produce IL-10 and to suppress LcT effectors proliferation by a cytokine dependent mechanism. Surprisingly, when monocytes were derived from allergic patients, the tolerogenic effect of CCL18 was lost, in association with a decreased binding of CCL18 to its putative receptor (Azzaoui I and al., in revision Blood) Moreover, we have shown that CCL18 may also play a role in the resolution of the allergic reaction with a chemotactic effect, by recruitment of a subpopulation of regulatory T cells CD4+CD25highCD127lowLAP+ (Chenivesse C et al., in revision JI). The effect of corticosteroids on CCL18 expression was analyzed. These results showed that the secretion of CCL18 induced by cytokines IL-4 and IL-10 is potentiated by dexamethasone (Chabrol J et al., in preparation) which confirms the anti inflammatory role of CCL18. The last study was an approach in a murine model of allergic asthma induced by ovalbumin in mice Balb/cByJ. Intratracheal administration of recombinant CCL18 to sensitized animals, inhibits asthmatic reaction development, by decreasing pulmonary inflammation (reduced eosinophil infiltration, and inhibition of local production of Th2 cytokine) and protects them against the deterioration of their respiratory function (protection against bronchial hyperresponsiveness, and inhibition of mucus hypersecretion). However, the cellular mechanisms behind this protection appear independent of major regulatory pathways of the reaction (J Gilet et al., in preparation). All these studies show, for the first time, that a chemokine is able to induce a tolerogenic response. However, this feature is absent in allergic donors who exhibit a defect in the binding of CCL18 to its putative receptor. This may participate to the lack of tolerance response observed in allergic diseases. This data suggest that CCL18 and its putative receptor may represent therapeutic targets
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Qaseem, Asif Shehzad. "Modulation of immune cell functions by human lung surfactant protein SP-D in allergic asthma." Thesis, Brunel University, 2016. http://bura.brunel.ac.uk/handle/2438/13893.
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Lung surfactant protein D (SP-D) is a soluble pattern recognition and innate immune molecule, which has been shown to be protective against lung infection, allergy, asthma and inflammation. SP-D is composed of an N-terminal collagen region and a homotrimeric, C-terminal carbohydrate binding domain (CRD). A recombinant form of trimeric CRD region (rhSP-D) has been shown to offer protection against asthma and inflammation in murine models by bringing down IgE levels, eosinophilia, and causing T helper cell polarisation from a pathogenic Th2 to a protective Th1 phenotype. Thus, rhSP-D can provide a therapeutic effect by dampening asthmatic symptoms in mice. The therapeutic mechanisms include inhibition of allergen-IgE binding and histamine release by sensitized mast cells, downregulation of allergen/antigen-specific IgG and IgE antibodies, pulmonary and peripheral eosinophilia, a shift from Th2 to Th1 cytokine response, interference with airway remodelling processes, and apoptosis- induction in sensitised eosinophils from allergic patients. The majority of the ex vivo and in vivo studies where a therapeutic effect of rhSP-D has been reported can not be explained by hitherto described candidate receptor involvement, especially CD91-calreticulin complex that requires collagen region for its cellular response. Thus, it is pertinent to examine at the cellular and molecular level how a trimeric lectin domain of human SP-D modulates immune cells. This was achieved by firstly expressing, purifying and characterising the recombinant rhSP-D and examining the interaction of rhSP-D with various immune cells such as macrophages, which are potent antigen presenting cells and play a crucial role in the maintenance of the inflammatory and humoral response to allergens. The highlight of this study is the demonstration that rhSP-D interferes with the co-operative binding of allergen-IgE complexes to B cells, and also downregulates expression of CD23, a low affinity IgE receptor (FcεRII), found on B cells. This suggests that inhibition of IgE-facilitated antigen presentation may represent a mechanism whereby SP-D suppresses Th2-driven allergic inflammation. In addition, this study is also the first to establish the calcium-dependent interactions between rhSP-D, CD23 and CD21. The possibility of formation of a trimolecular complex on the B cell surface may account for the suppression of IgE in therapeutic murine models since rhSP-D may interfere with CD21-CD23 mediated IgE production by primed B cells.
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Lorgat, Faizel. "Proliferative and cytotoxic cellular immune responses in human tuberculosis." Thesis, University of Cape Town, 1992. http://hdl.handle.net/11427/26373.
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Eliasson, Hanna. "Development of immunological methods and Real-Time PCR for detection of Macadamia nut (Macadamia spp.)." Thesis, Uppsala University, Department of Medical Biochemistry and Microbiology, 2005. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-6150.
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<p>A new European labeling directive (2003/89/EC) states that certain foods and products derived thereof must always be declared. Among the tree nuts specified is Macadamia nut (Macadamia spp.). During the last few years, cases of IgE-allergic reactions, even severe anaphylaxes, have been reported. Reliable methods for the detection of this nut are needed.</p><p>Protein from Macadamia nuts was isolated. Polyacrylamide gel electrophoresis in SDS revealed two main protein bands of about 20 and 50kDa. These protein bands were cut and extracted from the gel and rabbits were immunized with each protein.</p><p>Immunoblotting showed dominant reactivity with the respective antigens. The antisera were further tested for specificity in immunodiffusion and in rocket immunoelectrophoresis.</p><p>In addition, a specific DNA-method was developed, based on Real-Time PCR using Macadamia vicilin as target sequence. Two different primer pairs were tested. Specificity was tested against potentially related nuts. Optimisation of primer and probe concentrations was performed. The limit of detection was 2-4 pg DNA, corresponding to a macadamia nut concentration of 50 to 100 μg per g. In a background of soybean DNA, down to 0,01 % macadamia DNA could be detected.</p>
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Mhike, Morgen. "Characterization of Methylene Diphenyl Diisocyanate Protein Conjugates." PDXScholar, 2014. https://pdxscholar.library.pdx.edu/open_access_etds/1844.
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Diisocyanates (dNCO) such as methylene diphenyl diisocyanate (MDI) are used primarily as cross-linking agents in the production of polyurethane products such as paints, elastomers, coatings and adhesives, and are the most frequently reported cause of chemically induced immunologic sensitization and occupational asthma (OA). Immune mediated hypersensitivity reactions to dNCOs include allergic rhinitis, asthma, hypersensitivity pneumonitis and allergic contact dermatitis.
There is currently no simple diagnosis for the identification of dNCO asthma due to the variability of symptoms and uncertainty regarding the underlying mechanisms. Immunological sensitization due to dNCO exposure is traditionally thought to require initial conjugation of the dNCO to endogenous proteins to generate neoantigens, which trigger production of dNCO specific T lymphocytes and ultimately dNCO specific IgE. Testing for dNCO-specific IgE, for diagnosis of dNCO asthma is however, only specific (96-98%) but not sensitive (18-27%). The low prevalence of detectable dNCO specific IgE has been attributed to both assay limitations and a potential IgE-independent dNCO asthma mechanism(s). The identity of the conjugated proteins responsible for the sensitization also remains unknown. It is also not clear whether dNCOs bind to extracellular, cell membrane, or intracellular proteins as a way of triggering non-IgE asthma. Standardization and optimization of immunoassays used to screen for dNCO specific antibodies in sera is important if its utility as a dNCO asthma diagnostic tool is to be achieved. This will potentially improve sensitivity and allow comparison of results across studies. Current studies on assays of dNCO-specific IgE and IgG lack or have limited characterization of the conjugates used.
Diisocyanates bound to hemoglobin (Hb), human serum albumin (HSA), and THP-1 proteins were quantified by HPLC with fluorescence detection. Proteomic tandem mass spectrometry (MS) was used to delineate TDI and MDI specific amino acid binding sites on Hb as well as identification of proteins from MDI exposed THP-1 cells. The trinitrobenzene sulfonic acid assay (TNBS) and SDS gel electrophoresis were used to evaluate extent of intra and intermolecular cross-linking in dNCO-HSA conjugates. Binding of monoclonal antibodies (mAbs) to dNCO bound proteins in enzyme-linked immunosorbent assay (ELISA) was used to evaluate antigenicity of dNCO-protein conjugates.
The amount of dNCO binding to HSA and Hb increased with the concentration of the dNCO used for conjugation. All the dNCOs reacted with HSA more than with Hb. Eight binding sites were observed with both MDI and TDI on Hb. The N-terminal valines of both the alpha and beta subunits on Hb, lysine 40 of the alpha subunit and lysine 61 of the beta subunit were common binding sites for both TDI and MDI. Lysine 7 of the alpha subunit and lysines 8, 65 and 66 of the beta subunit were unique to MDI. On the other hand, lysines 11, and 16 of the alpha subunit and lysines 17 and 144 of the beta subunit were unique to TDI. Protein bound MDI was detected in a dose-dependent manner in membrane and cytoplasm fractions of MDI exposed THP-1 cells. MDI was also detected in 11 of the 13 cytoplasmic protein bands. The extent of MDI intracellular protein binding was not affected by cytochalasin D, a chemical that binds actin filaments and inhibits active uptake into cells. The extent of cross-linking shown using the TNBS assay was found to increase with amount of dNCO used. Clear bands from both intra and intermolecular cross-linking were observed on all dNCO-Hb/HSA SDS gels. Using ELISA, both TDI-Hb and TDI-HSA conjugates were reactive to monoclonal antibodies produced against TDI conjugated HSA indicating that dNCO-Hb is also antigenic.
The best characterization of dNCO-protein conjugates is achieved by the quantitative determination of conjugated dNCO per mole of protein as well as determining the extent of dNCO cross-linking. Although HSA is more reactive to dNCOs than other serum proteins such as Hb, contribution from other serum proteins to development of OA should not be overlooked as dNCO-Hb was found to be reactive to dNCO specific mAbs. dNCO-conjugated proteins identified in the soluble fraction of MDI exposed THP-1 cells were all of intracellular origin suggesting that MDI can cross the cell membrane and react with intracellular proteins. The entry of MDI into live cells is a passive process, as the extent of intracellular binding was not affected by cytochalasin D. The present study support the potential involvement of dNCO-haptenated membrane and intracellular proteins in development of non-IgE dNCO asthma.
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Wu, Qi Xuan. "Immunobiology of peptides from venom of the jumper ant Myrmecia pilosul." Thesis, The University of Sydney, 2001. https://hdl.handle.net/2123/28045.
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Ants from genus Myrmecia, subfamily Myrmeciinae, are aggressive stinging insects with medical importance in Australia, especially in the endemic areas of southeast Australia and Tasmania. Venoms of Myrmecia ants can cause allergic reactions with symptoms ranging from local to systemic. In some sensitized individuals of extreme severity, even death can occur. Two major allergens, Myr p 1 and Myr p 2 had been cloned and characterized from venom of one species, Myrmecia pilosula. The aim of this thesis was to study several aspects of the allergens from venoms of Myrmecia ants.
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Hillson, William Rawstron. "The role of thermal processing and protein oxidation in peanut allergy." Thesis, University of Oxford, 2013. http://ora.ox.ac.uk/objects/uuid:88d64b79-a7e6-4e41-acee-47c215d39f6b.
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Food allergies are an increasing health problem throughout the developed world. Among these, peanut allergy is particularly significant, due to its exceptional severity and frequent lifelong duration. Much of its aetiology remains unclear. In particular, it remains unknown why, unlike other food allergies, peanut allergy incidence correlates poorly with average dietary peanut consumption. A popular explanation for this discrepancy is that peanut allergy is more common in regions where predominantly dry-roasted (DR) peanuts are consumed, leading to speculation that DR-induced chemical modifications may contribute to pathological T<sub>h</sub>2 responses in humans. Yet to date, no research group has demonstrated an enhanced immunogenicity of DR peanuts relative to raw in a murine model of sensitisation. This thesis begins with the hypothesis that dry-roasting does indeed alter the chemical composition of peanut proteins in such a way as to increase immunogenicity and allergenicity. To test this hypothesis robustly, I have first addressed flaws in previous studies by developing a methodology to thoroughly characterise samples of raw and DR peanut protein, as well as purifying samples of individual peanut allergens. Using these samples, I have demonstrated an enhanced immunogenicity of DR peanut protein relative to raw, in intragastric, subcutaneous and epicutaneous models of mouse sensitisation, and furthermore, that such enhanced responses feature a pronounced T<sub>h</sub>2 bias and functional IgE production. I will present evidence that this difference is not caused by either protein aggregation or the presence of other non-protein substances, but is due to an intrinsic property of the DR peanut proteins. I will go on to clarify candidate molecular mechanisms of this effect, examining several putative receptors and probing the effects of roasting on dendritic cell binding and interactions of peanut proteins. I conclude in light of these investigations that the dry-roasting hypothesis remains the most plausible explanation for the epidemiological distribution of peanut allergy, although many additional questions remain regarding the nature of the chemical modifications produced by roasting and the molecular basis of their recognition by the immune system.
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Oliveira, Raquel Soares Binotti de. "Atividade acaricida contra ácaros Dermatophagoides pteronyssinus e D. farinae (Pyroglyphidae) de produto contendo óleos essenciais de Lavadula officinalis e Mentha piperita (Labiatae)." [s.n.], 2009. http://repositorio.unicamp.br/jspui/handle/REPOSIP/308185.
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Orientador: Ângelo Pires do Prado<br>Tese (doutorado) - Universidade Estadual de Campinas, Faculdade de Ciências Médicas<br>Made available in DSpace on 2018-08-16T09:23:48Z (GMT). No. of bitstreams: 1
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Previous issue date: 2009<br>Resumo: Ácaros são os principais agentes relacionados ao quadro de sensibilização respiratória de indivíduos atópicos no Brasil, sendo responsáveis por crises de asma, rinite e conjuntivite alérgicas, dentre outros. São encontrados nas residências principalmente em colchões, sofás e tapetes, onde alguns métodos podem ser utilizados para controlar sua infestação. O objetivo desse estudo foi o de avaliar a eficácia acaricida in vitro do produto a base de óleo essencial das plantas Lavandula officinalis e Mentha piperita (Labiatae) contra ácaros Dermatophagoides pteronyssinus e Dermatophagoides farinae (Pyroglyphidae). O efeito acaricide do Produto-Teste foi comparado com vários outros produtos químicos em estudos in vitro e de intervenção. O estudo in vitro foi
realizado utilizando culturas acarinas, nas quais os produtos foram diretamente aplicados e em placas de Petri onde um número de ácaros foram colocados em contato com as substâncias testadas. A mortalidade acarina foi avaliada e utilizada
para a comparação. O estudo de intervenção foi realizado em 30 residências de pacientes atópicos com asma e/ou rinite. A eficácia do Produto-Teste foi comparada com um produto acaricida comercializado no país através da quantificação de alérgenos acarinos Der p1 e Der f1 por ELISA e pela contagem do número de corpos acarinos nas amostras de poeira coletadas de colchões, sofás e tapetes tratados com um dos produtos pelo período de 6 meses. As implicações clínicas como sintomas alérgicos e segurança aos humanos dos produtos também foram avaliados. O estudo in vitro demonstrou que o efeito acaricida do Produto-Teste foi similar aquele observado com os produtos químicos. No estudo de intervenção, houve uma diminuição significativa nas concentrações dos alérgenos Der p1 e Der f1 nos 3 substratos tratados. Essa diminuição foi semelhante aquela observada com o produto comercial utilizado como controle. Apesar dos resultados, o número de corpos acarinos nas amostras de poeira dos 3 substratos não demonstrou alteração significativa após os 6 meses de tratamento para ambos os produtos testados. Além disso, os produtos foram considerados seguros para uso humano, desde que não foram observados efeitos adversos ou sinais de irritação significativos, embora fosse observado que alguns patientes atópicos presentes no recinto quando da aplicação do produto reclamaram de sintomas respiratórios. Os resultados demonstram que o acaricida contendo óleos essenciais de Lavandula officinalis e Mentha piperita (Labiatae) apresenta significativo efeito in vitro contra ácaros Dermatophagoides pteronyssinus e Dermatophagoides farinae (Pyroglyphidae) e causa uma diminuição significativa nos níveis de Der p1 e Der f1 na poeira de colchões, sofás e tapetes tratados. O produto foi considerado seguro para uso por humanos.<br>Abstract: House dust mites (HDM) are the greatest source of indoor allergens in Brazil, being closely implicated in respiratory allergic diseases such as asthma and rhinitis. In dwellings, HDM allergens are mainly found on mattresses, sofas and rug surfaces, where several methods such as mattress-covers and acaricides, can be used to control indoor mite infestation. The aim of this study was to evaluate the acaricide effect of an herbal product containing essential oils from Lavandula officinalis and Mentha piperita (Labiatae) against mites Dermatophagoides pteronyssinus and Dermatophagoides farinae (Pyroglyphidae). The acaricide effect of the Test-product was compared with several other chemical products in in vitro and clinical studies. The in vitro study was conducted using mite cultures, in which the chemical products were directly applied and in Petri dishes where a number of mites were placed in contact with the chemicals tested. Mite mortality was counted and used as comparison. The clinical study was conducted in 30 dwellings of atopic patients with asthma and/or rhinitis. The efficacy of the Test-product was compared with a Brazilian commercial acaricide and was done by ELISA quantification of the mite allergens Der p1 and Der f1 and by the number of body mites on dust collected from a mattress, sofa and rug treated with one of the products for 6 months. Clinical implications in allergic symptoms and the toxicity of the products for humans were also evaluated. The in vitro study showed that the acaricide effect of the Test-product was similar to that observed with the chemical products. In the clinical study, a significant decrease in Der p1 and Der f1 allergens concentrations were observed in all 3 treated sources. This decrease was similar to that observed with the commercial product used as control. Despite these results, the number of mite bodies on dust from all 3 sources presented no significant difference after the 6- months of treatment for both Test- and Control-products. Also, both products were considered safe for human use, since no significant adverse effects or toxicity signals were observed, although, atopic patients who were present in the room when the product was applied complained of respiratory symptoms. Our findings showed that the acaricide containing essential oils from Lavandula officinalis and Mentha piperita (Labiatae) has a significant in vitro effect against mites Dermatophagoides pteronyssinus and Dermatophagoides farinae (Pyroglyphidae) and caused a significant decrease in Der p1 and Der f1 levels on dust from treated mattresses, sofas and rugs. The product was considered safe for human use.<br>Doutorado<br>Saude da Criança e do Adolescente<br>Doutor em Saude da Criança e do Adolescente
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Lu, Thomas X. "MicroRNA in the Pathogenesis of Allergic Inflammation." University of Cincinnati / OhioLINK, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1329935942.
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Travers, Jared. "Altered Esophageal Epithelial Differentiation in EoE and Regulation of IL-1 Cytokine Responses by Chromatin." University of Cincinnati / OhioLINK, 2017. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1504802854888675.
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Sjögren, Ylva Margareta. "Early-life gut microbiota and breast milk oligosaccharides in relation to childhood immune maturation and allergy." Doctoral thesis, Stockholms universitet, Wenner-Grens institut för experimentell biologi, 2009. http://urn.kb.se/resolve?urn=urn:nbn:se:su:diva-26781.
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Atopic allergy is the most common chronic disease among children in the developed world. This high prevalence could be associated with low microbial exposure. The early gut microbiota appears to be important for immune maturation. Immunomodulatory components in human milk might differ between mothers and could therefore explain the contradictory results seen regarding breastfeeding and allergy development. The aim of this thesis was to investigate whether early colonization with certain gut microbiota species influences childhood immune responses and allergy development up to age five. Also, as human milk oligosaccharides (HMOs) might stimulate the growth of certain gut microbiota species, the consumption of neutral colostrum HMOs was investigated for their role in allergy development up to 18 months. The concentrations of neutral colostrum HMOs varied considerably between women; however this variation could not be explained by their allergic status. Neither was the consumption of neutral colostrum HMOs related to allergy development in their children up to 18 months. Infants who harboured lactobacilli group I and Bifidobacterium adolescentis one week after birth developed allergic disease less frequently during their first five years than infants who did not harbour these bacteria at the same time. Also, colonization with several Bifidobacterium species was associated with higher levels of house dust endotoxin and larger family size. The early Bifidobacterium flora influenced levels of salivary secretory IgA at six and 12 months but not during later childhood. Moreover, the intensity of early Bacteroides fragilis colonization was inversely associated with spontaneous Toll-like receptor 4 mRNA expression in peripheral blood cells collected 12 months after birth. In conclusion, these results indicate that the early infant gut microbiota influences systemic and mucosal immune maturation during infancy, and that it might be altered in infants developing allergic disease.
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Raman, Kavita. "Regulation of interferon-gamma production in human peripheral blood mononuclear cells: Heredity, relation to markers of allergy and possible role of inducible T cell kinase (ITK)." Diss., The University of Arizona, 2000. http://hdl.handle.net/10150/289221.
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IFN-γ and IL-4 are cytokines that are thought to be products of distinct differentiation pathways for lymphocytes and that inhibit and enhance the development of IgE antibodies, respectively. We hypothesized that the level of IFN-γ production upon stimulation of immune cells in the blood is a stable, heritable phenotype that is inversely related to phenotypic markers of allergy and to the Th2 cytokine IL-4. The studies were performed with samples of human blood obtained from children enrolled at birth in a large, longitudinal study of allergy known as the Tucson CRS. Mitogen-stimulated IFN-γ production by PBMCs of children at age 11 was compared to IFN-γ production in the first year of life and found to show a significant positive correlation. The expected inverse relation to markers of allergy (total serum IgE, skin test reactivity and eosinophils) was not observed. A strong positive relation was observed between IFN-γ production in the parents and children, lending support to the concept of genetic regulation. In contrast to the inverse relation hypothesized to IL-4, a positive relation was observed to IL-4 as well as to another cytokine, IL-2. A linkage analysis performed by a colleague showed linkage between low production of IFN-γ and a region of chromosome 5q in which the gene for a T-cell specific kinase (Itk) is located. These results led us to hypothesize a common "regulator" of cytokines that was functioning and might be Itk. Decreased expression and/or decreased function of Itk could account for the low cytokine data. In order to test this hypothesis, ten adult volunteers with low and ten with high cytokine production matched for age and sex were tested for Itk function and expression. The two groups were examined for Itk expression (normalized to CD3 expression) by western blotting. The group of low cytokine producing individuals showed significantly less Itk expression than the high cytokine-producing group. Attempts to optimize an in vitro kinase assay to determine Itk function were unsuccessful. In the absence of functional studies to support the results from the expression studies, it is not possible to say with certainty that Itk function is related to cytokine production. Therefore, we conclude that IFN-γ expression in humans is a stable phenotype with evidence of a genetic basis for regulation and that Itk is a candidate gene contributing to that genetic basis.
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Reddy, Keerthi C., Mary Kearns, S. Alvarez-Arango, et al. "YouTube and Food Allergy: An Appraisal of the Educational Quality of Information." Digital Commons @ East Tennessee State University, 2016. https://dc.etsu.edu/etsu-works/115.
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Coley, Rose Michelle. "The Association of Cancer Development in Patients with Systemic Lupus Erythematosus." ScholarWorks, 2016. https://scholarworks.waldenu.edu/dissertations/2148.
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The Association of Cancer Development in Patients with Systemic Lupus Erythematosus by
Rose Michelle Coley
MPH, Walden University, 2011
BS, University of Mount Olive, 2008
Dissertation Submitted in Partial Fulfillment
of the Requirements for the Degree of
Doctor of Philosophy
Public Health
Walden University
March 2016
Both cancer and autoimmune diseases have been associated with numerous factors that may independently lead to the development of either disease. When these factors overlap the difficulty in assessing association is compounded. The numerous factors that are thought to cause systemic lupus erythematosus (SLE), which leads to the development of cancer, makes the study of an association between the 2 diseases challenging. The purpose of this study was to examine whether the risk of cancer development increased in SLE patients compared to the risk in non-SLE patients. Researchers have not shown consistent relationships of cancer development in patients with SLE; however, consideration of the various factors that contribute to the diseases is necessary to measure an association between the 2 diseases. This study used the Clinical Practice Research database (CPRD), a large, population-based database to test the relationship between SLE and cancer. A matched retrospective cohort study among SLE (n=3025) and non-SLE (n=180555) patients was conducted using the propensity score methodology to help balance the differences between the comparison groups. The propensity score methodology created a similar distribution of observed baseline covariates between the 2 groups. With adjustment for age, the predictor variable of SLE indicates that a patient with SLE is still 2.7 times more likely to develop cancer than is a non-SLE patient. The study outcomes could promote positive social change by reinforcing current recommendations for cancer screenings in persons with SLE, which could enhance the ability to detect cancer early enough to decrease mortality because of cancer in persons with SLE.
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Medeiros, Marcell Costa de. "Modulação da imunidade adaptativa por produtos solúveis de células de carcinoma espinoceular de cabeça e pescoço (HNSCC) : um papel da galanina derivada do tumor? /." Araraquara, 2016. http://hdl.handle.net/11449/138922.
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Orientador: Carlos Rossa Junior<br>Banca: Alexandra Ivo de Medeiros<br>Banca: Luis Carlos Spolidorio<br>Banca: Ricardo Della Coletta<br>Banca: Roseanas Almeida Freitas<br>Resumo: Carcinoma espinocelular de cabeça e pescoço (HNSCC, squamous cell carcinoma of the head and neck) é uma neoplasia caracterizada mais comumente por invasão local/regional de prognóstico sombrio quando diagnosticada em estágios avançados e uma característica imunossupressão local ou sistêmica associada. A taxa de sobrevivência em casos avançados é inferior à de câncer de mama ou próstata, e seu tratamento usualmente causa morbidade severa. A resposta ao tratamento é altamente variável mesmo entre pacientes em estágios iniciais da doença e apesar do tratamento implementado seguir o padrão de cuidados vigente. Assim, há grande necessidade de identificar biomarcadores que indiquem um fenótipo agressivo e possa proporcionar informações de utilidade no desenvolvimento de novas terapias específicas. Nossa hipótese foi de que produtos secretados por células de HNSCC ou o contato direto das mesmas com células imunológicas podem induzir uma modulação no sentido de causar a evasão do tumor da resposta imune. Observamos que a literatura mostra diversos trabalhos onde células tumorais exercem efeito imunossupressor em diversos tipos celulares da resposta imune. O estímulo de PBMC com meio condicionado (CM) de células de HNSCC induziu uma diminuição na proliferação, bem como modulou a polarização para fenótipos anti-inflamatórios e em co-cultura de HNSCC e PBMC, o tratamento prévio com CM das PBMC conferiu vantagem às células tumorais. Por último avaliamos um possível biomarcador, a galanin... (Resumo completo, clicar acesso eletrônico abaixo)<br>Abstract: Squamous cell carcinoma of head and neck (HNSCC) is a cancer characterized commonly by local/regional invasion of poor prognosis when diagnosed in advanced stages and are associated with local or systemic immunosuppression. The survival rate for advanced cases is below the breast or prostate cancer, and treatment usually causes severe morbidity. The response to the treatment is highly variable among patients even in the early stages of the disease, despite the treatment implemented following the current standard care. Thus, there is great need to identify biomarkers that indicate an aggressive phenotype and can provide useful information on the development of new target therapies. Our hypothesis was that secreted products by HNSCC cells or direct contact with immune cells can induce a modulation in order to cause tumor evasion of the immune response. We note that the literature shows several studies where tumor cells exert immunosuppressive effect in different cell types of the immune response. The stimulation of PBMC with conditioned medium (CM) of HNSCC cells induced a decrease in proliferation, and modulates a polarization toward anti-inflammatory phenotypes and in co-culture of HNSCC and PBMC pre-treatead with CM caused advantage to tumor cells. Finally we evaluate a possible biomarker, galanin, in modulating the immune response. The absence of galanin induced higher levels of proliferation as well a more bias towards proinflammatory phenotypes. Increase of galanin expres... (Complete abstract click electronic access below)<br>Doutor
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Burgess, Stacey L. "A specific component of the intestinal microbiota exacerbates the severity of allergic asthma." University of Cincinnati / OhioLINK, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1368026710.
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Yamani, Amnah. "Dysregulation of Vascular Endothelial Function Modulates Severity of IgE-mediated Anaphylactic Reactions." University of Cincinnati / OhioLINK, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1490350649626552.
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Lotfi-Emran, Sahar. "Transformation of human mast cells by interferon-gamma and the potential role of myeloid derived suppressor cells in mastocytosis." VCU Scholars Compass, 2014. http://scholarscompass.vcu.edu/etd/4077.
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Mast cells respond to a variety of signals, are associated with both increased inflammation and regulation of the immune response, and are able to interact with a variety of hematopoietic and non-hematopoietic cells. The majority of the work that highlights mast cell pleiotropic abilities has been completed in murine models. Though these models have significantly advanced our understanding of what mast cells can do, they cannot inform us as to what mast cells actually do in human beings. The goal of this dissertation is to assess fully mature, primary human mast cell function beyond the well-defined type 1 hypersensitivity function and place mature human mast cells in the context of interactions with other immune cells. The first project addresses the ability of IFNγ, a historically Th1 associated cytokine, to dramatically alter mast cell phenotype. In particular, IFNγ stimulation allows mast cells to act as antigen presenting cells to CD4+ T cells. The second project describes and addresses the T cell suppressive function of myeloid derived suppressor cells in Mastocytosis, a disease of clonal mast cells.
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Noakes, Paul Stanton. "The effects of maternal smoking on infant immune development." University of Western Australia. School of Paediatrics and Child Health, 2006. http://theses.library.uwa.edu.au/adt-WU2006.0080.
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[Truncated abstract] With the dramatic rise in asthma and allergic disease there is an urgent need to define the early life exposures which influence developing immune responses to increase the predisposition to allergic disease. While this is clearly multifactorial, this thesis addresses the effects of maternal smoking as a major adverse, yet avoidable exposure in early life. I hypothesised that the well-documented increased susceptibility to infection in infants of smokers could indicate underlying effects on innate Toll-like receptor (TLR) mediated microbial responses which could in turn contribute to early immune dysregulation and increased risk of allergic disease. In addition to providing the first defence against microbes, TLR-mediated pathways modulate subsequent specific immune response and are of growing interest in the potential inhibition of inappropriate allergic responses. My initial interest in the potential immune effects of smoking in pregnancy was based on preliminary retrospective analyses of a previous cohort (presented in Chapter 3) which suggested possible effects on T cell cytokine responses to mitogens and allergens. Based on this, I recruited a new prospective pregnancy cohort (n=122) of smokers (n=60) and non-smokers (n=62) (as outlined in Chapter 4) to confirm this and test my novel hypothesis that maternal smoking may be affecting important innate (TLR-mediated) immune pathways. … Thus, these findings could indicate that smoking increases the early susceptibility to infection thereby increasing subsequent IgA responses. This is supported by observations that key neonatal TLR responses are attenuated in children who go onto develop wheezy illnesses and lower respiratory tract infections. Together, the study findings suggest that in addition to effects on lung growth, maternal smoking may also influence aspects of neonatal innate immune function that are now believed to play a critical role in microbial-driven postnatal immune development, highlighting that other environmental interactions are also highly relevant to the v
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Yokoyama, Nicole Hune. "Sensibilização ao extrato de Blomia tropicalis, na ausência de alum, requer a molécula adaptadora MyD88." Universidade de São Paulo, 2014. http://www.teses.usp.br/teses/disponiveis/42/42133/tde-11072014-111650/.
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Exposição a alérgenos de poeira doméstica é fator de risco para o desenvolvimento de doenças alérgicas. Os objetivos foram estudar a resposta inflamatória pulmonar alérgica induzida pela sensibilização i.n. ou s.c. ao extrato do ácaro Blomia tropicalis (Bt) e avaliar a participação da molécula adaptadora Myd88. Animais C57BL/6 sensibilizados com solução de extrato de Bt adsorvido ao alum exibiram altos níveis de IgE e aumento do número de eosinófilos. Contudo, animais sensibilizados apenas com Bt não apresentaram aumento dos níveis de IgE. Assim, animais C57BL/6 ou MyD88KO foram sensibilizados com uma dose maior do extrato de Bt (i.n. ou s.c.) e desafiados i.n. As sensibilizações produziram aumento do número células no BAL e níveis de IgE. Os parâmetros celulares em animais MyD88KO se mostraram inibidos, contudo, os níveis de IgE foram similares aos dos animais WT. Concluindo, o desenvolvimento de inflamação pulmonar alérgica não requer alum e sensibilização i.n. ou s.c. induz o recrutamento de células, dependente de MyD88 e produção de IgE, independe de MyD88.<br>Exposure to allergens from house dust is a risk factor for the development of allergic diseases. The objectives were to study the allergic lung inflammatory response induced by sensitization i.n. or s.c. to Blomia tropicalis (Bt) extract and determine the role of MyD88 adapter molecule. C57BL/6 mice sensitized with Bt extract solution adsorbed to alum exhibited high levels of IgE and increased numbers of eosinophils. However, animals sensitized only with Bt did not show increased levels of IgE. Thus, C57BL/6 or MyD88KO mice were sensitized with a higher dose of Bt extract (i.n. or s.c.) and challenged i.n. The sensitization produced increased cell number in BAL and IgE serum levels. Cell parameters were inhibited in MyD88KO mice, however, IgE levels were similar to those of WT mice. In conclusion, the development of allergic lung inflammation does not require alum, i.n. or s.c. sensitization induces cell recruitment dependent of MyD88 adaptor molecule and IgE production is independent of MyD88.
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Gudimetla, Vishnu. "Mechanisms of Allergic Sensitization and Desensitization in a Mouse Model." University of Cincinnati / OhioLINK, 2017. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1529667182585476.
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Gonzalez, Tammy. "Investigating the Role of the Human Microbiome in the Pathogenesis of Atopic Dermatitis in the Mechanisms of the Progression of Atopic Dermatitis to Asthma in Children (MPAACH) Cohort." University of Cincinnati / OhioLINK, 2020. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1593268717032036.
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Victor, Jefferson Russo. "Mecanismos regulatórios mediados pelos anticorpos maternos na modulação da resposta de hipersensibilidade do tipo I ao alérgeno ovalbumina em camundongos neonatos." Universidade de São Paulo, 2008. http://www.teses.usp.br/teses/disponiveis/42/42133/tde-25032009-171427/.
Full textAbstract:
Avaliamos os mecanismos regulatórios desencadeados pela imunização materna na resposta alérgica da prole OVA. A imunização materna com OVA promoveu alterações como o aumento da expressão dos receptores FcgRIIb nos linfócitos B esplênicos dos neonatos aos 3 dias de idade (d.i.), o que se manteve até os 20 d.i. Com a imunização das proles no período neonatal a imunização materna inibiu a produção de anticorpos IgE anti-OVA. Além disso, foi observado na população de linfócitos B da prole o aumento da expressão dos receptores FcgRIIb e CD44. A transferência passiva de IgG de mães imunes no pós-natal mostrou uma inibição da produção de IgE, e no período pré-natal foi capaz de reduzir a expressão das moléculas CD40 e CD23 nos linfócitos B e a secreção de IL-10 em linfócitos T CD4 na prole no período neonatal. As evidências mostram que a imunização pré-concepcional com OVA induz mecanismos que regulam a resposta IgE da prole imunizada no período neonatal, o que foi parcialmente observado com a transferência passiva de anticorpos IgG durante o período pré e pós-natal.<br>To evaluate the regulatory mechanisms triggered by maternal immunization in the immune response of the offspring, the effect of preconceptional immunization with OVA was evaluated. Maternal immunization with OVA led to early alteration with increased expression of FcgRIIb in B lymphocytes from 3 days old pups. Offspring from immune mother showed diminished percentage of CD4 T cells IL-4+. The immunization of offspring during neonatal period showed that maternal immunization inhibits the production of anti-OVA IgE antibodies. The evaluation of CD4 T cell population revealed diminished IL-4+ cells. Passive IgG transfer from immune mother during neonatal period showed inhibition in the IgE synthesis, during pregnancy showed capacity to reduce the expression of CD40 molecules in B cells from neonatal pups. These evidences show that maternal OVA immunization down regulates the IgE response of offspring including phenotypic and functional alteration in B and CD4 T cells. These alterations were partially observed with IgG transfer during pregnancy or after birth.
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Elliott, Alicia Rochelle. "Immunological techniques for the serum determination of specific-IgE levels among workers exposed to seafood allergens." Thesis, Cape Technikon, 2003. http://hdl.handle.net/20.500.11838/1473.
Full textAbstract:
Thesis (MTech (Biomedical Technology))--Cape Technikon, 2003<br>Allergic conditions among workers processing seafood are most often related to inhalation of
the seafood antigens or via direct unprotected handling of the seafood and its products. This
can cause sensitised individuals to suffer from asthma, rhino-conjunctivitis, urticaria and
protein contact dermatitis, which are IgE mediated. Food intolerance may also occur which is
a non-IgE mediated reaction, however the exact mechanism is yet to be determined. There is
therefore a need to develop reliable tests to identify sensitised workers processing seafood.
The objective of this study was to prepare specific seafood extracts from raw and cooked
lobster; raw and cooked saltwater bony fish species (mackerel, red eye, maasbanker, pilchard
and anchovy) and fishmeal dust obtained from a fish-processing factory. These extracts were
tested by SDS-Polyacrylamide Gel Electrophoresis to characterise the seafood proteins, and
the allergenicity was confirmed by the Western blot technique. Polyclonal IgG antibodies
were also successfully generated in rabbits, using the specific seafood extracts isolated from
the various species.
The second objective was to optimise and standardize an Enzyme Allergosorbent Test
(EAST) method to quantify specific IgE antibodies in the sera of factory workers. This EAST
was optimised and validated to detect allergen-specific IgE to each of the different fish
species and also one crustacean species (rock lobster). Sera from a group of workers were
selected and analysed for specific IgE antibodies by the optimised EAST (S) (South African
laboratory), and commercial RAST techniques. Analysis was performed for the three most
important extracts, pilchard (canned), anchovy, and lobster. The same samples were analysed
by EAST (R) in the reference laboratory (Dr Gerald Reese; Paul-Ehrlich-Institute, Germany).
The different techniques, and the EAST (R) and the EAST (S) results were compared by
using a statistical software package.
An EAST method was successfully developed, however, compared to the results obtained by
the reference laboratory the sensitivity and specificity was below 80%. The main reason for
the low agreement between the two laboratories was the fact that the South African laboratory
used a modified EAST method, and different data calculation methods, for categorising
positive results. The South African laboratory did not use a kit-based assay and a serum
dilution of 1:4 and not 1:2 were used when compared to the reference laboratory. When the
EAST results were compared to the RAST results, poor agreement was found due to the fact
that canned pilchard was used in the EAST while raw pilchard in the commercial RAST
assay. For pilchard, anchovy and lobster EAST, different species were utilized compared to
the RAST, and this can also explain the poor level of agreement.
Future directions would be to further standardise the EAST method and to introduce reference
sera and a standard curve to determine positive results, thereby ensuring more reproducible
results between laboratories.
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Groschwitz, Katherine R. "Mast cell-mediated intestinal barrier function in homeostasis and disease." University of Cincinnati / OhioLINK, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1291389792.
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Damle, Sheela Ruby. "TYPE 2 IMMUNE RESPONSES IN THE CONTEXT OF HELMINTH INFECTION, ASTHMA, DENDRITIC CELLS, AND MYELOID DERIVED SUPPRESSOR CELL FUNCTION." VCU Scholars Compass, 2017. http://scholarscompass.vcu.edu/etd/4696.
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Type 2 (TH2) immune responses evolved to respond to helminth parasite infections by the production of TH2 cytokines, which stimulate anti-helminth immunity. Macrophage migration inhibitor factor (MIF) is a pleiotropic cytokine, which is produced by many cell types. We demonstrate that mice deficient in MIF have enhanced clearance of a helminth parasite. MIF deficiency in CD4+ T cells was found to be the most important for mediating parasite clearance. We mimicked MIF deficiency by administering an inhibitor of the MIF tautomerase activity, sulforaphane, and this also increased parasite clearance (Section I).
TH2 immune responses underlie allergy and allergic asthma, in which the same cytokines that help expel parasites are released in response to innocuous substances. Integral to the initiation of adaptive TH2 immunity are dendritic cells (DCs), which take up antigen and stimulate antigen-specific CD4+ T cell responses. We found that DC expression of ADAM10, a zinc-dependent metalloproteinase, is critical for the development of TH2 immune responses and IgE production from B cells. This effect is demonstrated in both allergic airway inflammation and anaphylaxis models. ADAM10-deficient DCs are unable to cleave Notch1 receptors, resulting in reduced IL-6 production and this ultimately results in decreased TH2 activity. ADAM17 is closely related to ADAM10 in both structure and function. Interestingly, mice from which ADAM10 and 17 are removed from DCs (ADAM10/17DC-/-) have a distinct phenotype from both ADAM10DC-/- and ADAM17DC-/- mice in models of allergic airway inflammation (Section I).
We also examined another effect of TH2 cytokines on the interaction between mast cells and myeloid derived suppressor cells (MDSCs). We sought to understand how histamine and IL-13, mediators made by mast cells, affect the immunoregulatory function of MDSCs. MDSCs in IL-13-deficient mice with tumor are more prevalent in circulation rather than in tumor or organs, which could be due to changes in CCL2/CCR2 chemotaxis. In addition, MDSC function after treatment with the DNA methyltransferase inhibitor, decitabine was examined. This treatment reduced their suppressive function and increased the expression of molecules needed for antigen presentation. Overall, TH2 immunity has multifaceted roles in anti-parasite immunity, allergic asthma, and MDSC function (Section II).
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Vinot, Pierre-Axel. "Développement de pseudo-particules rétrovirales comme vaccin tolérogène et application dans l'allergie alimentaire." Thesis, Sorbonne université, 2018. http://www.theses.fr/2018SORUS268.
Full textAbstract:
L’incidence croissante des désordres immunitaires a motivé le développement de nouvelles approches permettant l’induction d’une tolérance immunitaire spécifique et maintenue dans le temps. S’inscrivant dans ce cadre, la vaccination tolérogène exploite les propriétés innées du système immunitaire pour rétablir la tolérance en visant spécifiquement les cellules dendritiques et les lymphocytes T régulateurs. Ce concept se confronte néanmoins à certaines limitations dues au besoin d’apporter l’antigène sous une forme particulière ou de manière combinée avec un signal de tolérance. En exploitant les propriétés natives des pseudo-particules dérivées de rétrovirus, nous avons mis au point une plateforme permettant de répondre à ces problématiques propres à la vaccination tolérogène. Par ce travail de thèse, l’objectif fut de démontrer la faisabilité de cette approche, en produisant et caractérisant des VLP exprimant l’ovalbumine au sein de la capside et présentant le CTLA-4 à leur surface. Par une étude fonctionnelle sur les cellules dendritiques et sur des cellules présentant une spécificité réactionnelle pour l’ovalbumine, nous avons démontré les propriétés tolérogènes de ces VLP. Ces propriétés ont par la suite été confirmées dans un modèle d’allergie alimentaire induite à l’ovalbumine chez la souris. Les résultats obtenus montrent pour la première fois que ces VLP tolérogènes permettent le contrôle de l’allergie alimentaire de manière spécifique et à long terme et fournissent la preuve de concept de leur utilisation. Les travaux entrepris permettent d’envisager l’utilisation de ces particules dans d’autres champs d’application et notamment les maladies auto-immunes<br>The increasing incidence of immune disorders has motivated the development of innovative approaches allowing the induction of a specific and long-lasting immune tolerance. Tolerogenic vaccination stands as one of those new therapies and exploits the innate properties of the immune system to restore tolerance by specifically targeting major players such as dendritic cells and regulatory T cells. Nevertheless, this concept faces certain limitations due to the need to provide the antigen in a particular form or in combination with a tolerance signal. By exploiting the native properties of pseudo-particles derived from retroviruses, we have developed a platform to answer those needs. With this thesis research, the objective was to highlight the feasibility of this approach by producing and characterizing VLPs expressing ovalbumin within the capsid and presenting CTLA-4 molecules on their surface. By functional studies on dendritic cells and on ovalbumin specific T cells, we highlight the tolerogenic properties of these VLPs. These properties were subsequently confirmed in a model of ovalbumin-induced food allergy in mice. The obtained results demonstrate for the first time that these tolerogenic VLPs allow the control of food allergy in a specific and long-lasting manner, thus supporting the proof of concept of their use. Additional work also makes it possible to consider the use of these particles in other fields of application and in particular autoimmune diseases
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De, Leon Maria P. "Immunological and molecular characterisation of major peanut allergens and their cross-reactive components in tree nuts." Monash University, Dept. of Pathology and Immunology, 2004. http://arrow.monash.edu.au/hdl/1959.1/9673.
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