Dissertations / Theses on the topic 'Perforin'
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Kägi, David. "The role of perforin protein in lymphocyte mediated cytotoxicity /." [S.l.] : [s.n.], 1993. http://e-collection.ethbib.ethz.ch/show?type=diss&nr=10050.
Full textUhl, Dieter. "Einfluss körperlicher Ausdauerbelastung auf Perforin und Granzyme-B-exprimierende Lymphozytenpopulationen." [S.l.] : [s.n.], 2002. http://www.freidok.uni-freiburg.de/volltexte/440.
Full textSemple, Patricia Lynn. "The role of the cytolytic mediators, granulysin and perforin, in tuberculosis." Doctoral thesis, University of Cape Town, 2008. http://hdl.handle.net/11427/12403.
Full textIncludes abstract.
Protective immunity against mycobacterial infection requires an effective cytolytic response, in addition to an intact Type l (Th1) cytokine pathway. Natural killer (NK) cells and cytolytic T-cells (CTL) are essential components of protective immunity against tuberculosis (TB) and mediate granule-dependent killing of infected cells. Granulysin, an antimicrobial protein, and perforin, a pore-forming molecule, have been found to co-localise in the granules of these two cell types. Granulysin has been shown to be directly cytotoxic to extracellular Mycobacterium tuberculosis (M.tb) and, together with perforin, is cytolytic against intracellular mycobacteria. This project evaluated the role of these two cytolytic mediators in TB.
Haeryfar, Seyed Mohammad Mansour. "Antiestrogens modulate the perforin/granzyme pathway of natural killer cell-mediated cytolysis." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape8/PQDD_0001/MQ45052.pdf.
Full textFraser, Stephanie A. "Regulation of Perforin-mediated lysis by two endogenous grandule proteins, Calreticulin and Chymase I /." abstract and full text PDF (UNR users only), 1999. http://0-gateway.proquest.com.innopac.library.unr.edu/openurl?url_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:dissertation&res_dat=xri:pqdiss&rft_dat=xri:pqdiss:9961145.
Full textCartwright, Adam. "Investigating the gasket function and perforin secretion of the natural killer cell immune synapse." Thesis, Imperial College London, 2014. http://hdl.handle.net/10044/1/24104.
Full textTinangon, Maria M. "Strategies to identify granzyme J /." abstract and full text PDF (UNR users only), 2001. http://0-gateway.proquest.com.innopac.library.unr.edu/openurl?url_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:dissertation&res_dat=xri:pqdiss&rft_dat=xri:pqdiss:1404986.
Full textBradley, Michael Joseph. "Role of CD44, Fas Ligand, and Perforin in the Cytotoxicity Mediated by Natural Killer Cells." Thesis, Virginia Tech, 1997. http://hdl.handle.net/10919/36792.
Full textMaster of Science
Rafatpanah, Baygi Houshang. "Immunogenetic analysis of patients with HTLV-I infection : associations with HLA, cytokine and perforin gene polymorphisms." Thesis, University of Manchester, 2003. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.488453.
Full textWoodsworth, Daniel. "Characterizing the granzyme-perforin pathway and its utility as a cell-to-cell delivery system for cellular therapeutics." Thesis, University of British Columbia, 2017. http://hdl.handle.net/2429/62073.
Full textScience, Faculty of
Graduate
Natarajan, Kshama. "Part I- cluster assembly in protein bound iron-sulfur clusters ; Part II- solution structural studies on the N-terminus perforin /." The Ohio State University, 1998. http://rave.ohiolink.edu/etdc/view?acc_num=osu1487951907957761.
Full textKhazen, Roxana. "Dissecting early mechanism of melanoma cell resistance to cytotoxic T lymphocyte attack." Thesis, Toulouse 3, 2016. http://www.theses.fr/2016TOU30007/document.
Full textHuman melanoma cells express various tumor antigens that are recognized by CD8+ cytotoxic T lymphocytes (CTL) and elicit tumor-specific responses in vivo. However, natural and therapeutically enhanced CTL responses in melanoma patients are of limited efficacy. The mechanisms underlying the failure of CTL effector phase against melanomas are still largely elusive. Our hypothesis is that the limited efficacy of CTL in their fight against tumors is the result of an unfavorable balance between CTL ability to kill tumors and an intrinsic tumor resistance to CTL cytolytic activity. During my thesis I focused on the molecular dynamics occurring at the lytic synapse in order to identify possible "early response-mechanism" of melanoma cells to CTL attack. Using a combination of cutting edge microscopy approaches and molecular tools, I showed that upon conjugation with CTL, human melanoma cells undergo an exacerbated late endosome/lysosome trafficking, which is intensified at the lytic synapse and is paralleled by cathepsin-mediated perforin degradation and deficient granzyme B penetration. Abortion of SNAP-23-dependent lysosomal trafficking, pH perturbation or impairment of lysosomal proteolytic activity restores susceptibility to CTL attack. Our results reveal an unprecedented strategy of melanoma cell "self-defense" at the immunologic synapse based on a lysosome secretory burst and perforin degradation at the lytic synapse. Interfering with this synaptic self-defense strategy might be instrumental to potentiate CTL-mediated therapies in melanoma patients
Chang, Eddie. "The role of perforin and chemokines in the pathogenesis of chronic corneal inflammation induced by herpes simplex virus type-1 infection." free to MU Campus, others may purchase, 2003. http://wwwlib.umi.com/cr/mo/fullcit?p3091911.
Full textLage, Denise 1979. "Doenças liquenoides da pele e mucosa oral = análise histológica e imuno-histoquímica = Lichenoid diseases of the skin and oral mucosa : histological and immunohistochemical analysis." [s.n.], 2014. http://repositorio.unicamp.br/jspui/handle/REPOSIP/312892.
Full textTese (doutorado) - Universidade Estadual de Campinas, Faculdade de Ciências Médicas
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Resumo: O líquen plano (LP) pode afetar a pele e/ou as mucosas. Histologicamente apresenta infiltrado linfo-histiocitário na junção epitélio-tecido conjuntivo e apoptose de células epiteliais basais. No LP oral (LPO), ocorre erosão frequente pela maior intensidade da necrose. O LP cutâneo (LPC) e o LPO apresentam características histopatológicas similares, mas o curso clínico é diverso. O LPC costuma ter seu curso limitado, enquanto o LPO é frequentemente recidivante. A erupção liquenoide a droga (ELD) desenvolve-se após semanas da ingestão do medicamento e a resolução do quadro é lenta após a interrupção, dificultando o diagnóstico diferencial com o LP idiopático. Os achados clínicos e histológicos podem ser indistinguíveis daqueles do LP, mas a patogênese da ELD não é conhecida. Diferenças locais no sistema imune da mucosa oral e pele poderiam explicar a diversidade no comportamento clínico do LP. Quanto à ELD, há poucas publicações sobre as alterações imunes que atuam no seu desenvolvimento. A citotoxidade celular é mediada, dentre outros mecanismos, por grânulos contendo granzima B e perforina, produzidos por linfócitos T citotóxicos e células natural killers. Com o objetivo de estudar a citotoxicidade celular na patogênese destas doenças, foram analisadas 29 amostras de LPO, 16 de LPC e 6 de ELD. Os cortes foram corados pela H&E e técnica de imuno-histoquímica, para a demonstração de linfócitos CD4 e CD8, macrófagos HAM 56+ e MAC 387+, granzima B, perforina e ICAM-1. As amostras de LPO apresentaram maior densidade de células granzima B+ e perforina+, em comparação às do LPC. Nos dois grupos de doenças, quanto maior era o número de células perforina+, maior era o de células granzima B+. Maior número de células CD4-positivas foi encontrado nas lesões ativas, quando comparado com o das regressivas, no LPO, mas não no LPC. À comparação entre o LPC e a ELD, quanto maior o número de células CD8-positivas, maior era o número de células que expressavam a perforina no grupo LPC. Quanto maiores eram os valores da granzima B, maiores os da perforina, no grupo LPC. Quanto maiores eram os valores da granzima B, maiores os de células apoptóticas agregadas, no grupo da ELD. Nas amostras do LPC, quanto maiores os valores das células T, maiores os dos macrófagos HAM56-positivos e vice-versa. Nas amostras da ELD, foi encontrada correlação negativa entre o número de células T e o de histiocitos jovens (MAC 387+). Havia correlação positiva entre o número de células T e o de células CD8, no grupo da ELD. O mesmo não ocorreu, no grupo do LPC. Concluindo, a expressão aumentada dos grânulos citotóxicos no LPO pode estar associada à maior gravidade da doença na mucosa. Os resultados favorecem um papel mais importante da granzima B e linfócitos TCD8+, no mecanismo patogenético da ELD, comparativamente com o da perforina, de maior importância no LPC. É possível que a ação da granzima B esteja ligada ao número abundante de clusters encontrado na ELD. Embora o LPC e a ELD apresentem semelhanças clínicas e histológicas, a etiopatogênese parece ser distinta
Abstract: Lichen planus (LP) can affect the skin and/or mucous membranes. Histologically it presents lymphohistiocytic infiltrate in the epithelium-connective tissue junction and apoptosis of basal epithelial cells. In oral LP (OLP), erosion occurs frequently by higher intensity of necrosis. Cutaneous LP (CLP) and OLP present similar histopathological features, but the clinical course is diverse. Spontaneous remission is common in CLP, but OLP follows a prolonged course, with periods of remission and relapse. Lichenoid drug eruption (LDE) develops after weeks of drug intake and the resolution of lesions is slow after drug discontinuation, hampering the differential diagnosis with (idiopathic) LP. Clinical and histological findings of LDE may be indistinguishable from those of LP, but LDE pathogenesis is poorly understood Local differences in the immune system of the skin and oral mucosa could explain the diversity in the clinical behavior of CLP and OLP. Regarding LDE, there are few publications on the immune changes that act in its development. Cellular cytotoxicity is mediated, among other mechanisms, by granules containing perforin and granzyme B, produced by cytotoxic T lymphocytes and NK cells. In order to study cellular cytotoxicity in the pathogenesis of these diseases, we analyzed 29 samples of OLP, 16 of CLP and 6 of LDE. The sections were stained for H&E and immunohistochemically targeted with CD4, CD8, HAM 56, MAC387, granzyme B, perforin and ICAM-1. OLP specimens exhibited higher density of cytotoxic granules (perforin and granzyme B) when compared with CLP. In both groups of diseases, the greater the number of perforin+ cells, the greater was the number of granzyme B+ cells. Increased number of CD4+ cells was found in active lesions as compared with the regressive ones in OLP but not in the CLP. The comparison between CLP and LDE revealed that the greater the number of CD8+ cells, the greater the number of cells expressing perforin in CLP group. The higher were the values of granzyme B, the higher the perforin values in the CLP group; the higher were the values of granzyme B, the higher the number of clusters of apoptotic cells in the LDE group. Within CLP group, the higher were the values of T cells, the greater the number of HAM56+ macrophages and vice versa. In LDE samples, negative correlation was found between the number of T cells and young histiocytes (MAC 387+). There was a positive correlation between the number of T cells and CD8 cells in LDE group, but not in CLP group. Concluding, increased expression of cytotoxic granules in OLP may be associated with greater mucosa severity. The results favor a greater role of granzyme B and CD8+ lymphocytes in the pathogenic mechanism of LDE, when compared with perforin, of greater importance in CLP. It is possible that the action of granzyme B is connected to the abundant number of clusters found in LDE. Although CLP and LDE present clinical and histological similarities, the etiopathogenesis appears to be distinct
Doutorado
Anatomia Patologica
Doutora em Ciências Médicas
Camiña, Tato Montserrat. "Estudio del papel de los genes perforin 1 (PRF1), caspase 8 (CASP8) y B-cell translocation gene 1 (BTG1) en esclerosis múltiple." Doctoral thesis, Universitat Autònoma de Barcelona, 2016. http://hdl.handle.net/10803/399348.
Full textThe study of the genetic basis of the diseases is key not only for a better and fast diagnostic of the diseases, but also for a better treatment. In recent years, many genes that confer susceptibility to MS have been discovered; however, many remain yet to be replicated in other populations. The main objective of this doctoral thesis is to confirm the involvement of the following genes in the susceptibility to MS: PRF1, CASP8 and BTG1. After performing SNP genotyping by allelic discrimination and expression studies by microarrays, among other studies, our results indicate that the three genes may contribute in a modest way to the susceptibility to MS. In the case of the PRF1 gene, we observed a strong association between this gene and the susceptibility to MS, mainly in males with PPMS forms. The results with the CASP8 gene suggest an association between this gene and the susceptibility to MS in patients with PPMS. In addition, we observed an association between the CASP8 gene and the course of MS. Finally, the results with the BTG1 gene suggest an association between this gene and the susceptibility to suffer MS in forms with relapse-onset course.
Mossu, Adrien. "Régulation de la survie des cellules dendritiques plasmacytoïdes dans un contexte inflammatoire non viral." Thesis, Besançon, 2015. http://www.theses.fr/2015BESA3011/document.
Full textPlasmacytoid dendritic cells (pDC) are specialized in type I interferons (IFN-I) secretion to control viral infections. However, these cells can also activate adaptive immune responses, and polarize T cells. Indeed, during chronic or uncontrolled inflammatory episodes, pDC can induce or maintain inflammatory syndromes and autoimmune diseases. So some mechanisms should exist to control the fonction of these cells. In an in vivo modcl of non viral inflammation induced by the injection a CD3-specific antibody (aCD3 Ab), we could observed pDC's apoptosis dependent of T cell activation in different lymphoid organs. Moreover, we could observe that this depletion of pDC was not associated with the cytokinic storm induced by the mitogenic effect after aCD3 Ab treatment. On the other hand our data shovved that CD8+ T cells and the perforin pathway in this acute inflammatory context are responsible for pDC depletion We also obtained the same results in other non viral inflammation settings such as graft versus host disease. Overall, these data suggesi that this regulation pathway could be used for therapeutic purposes, to control pDC survival and avoid their involvement in the physiopathology of autoimmune disorders like systemic lupus erythematosus, psoriasis, multiple sclerosis or type I diabetes
Novais, Fernanda Oliveira. "Avaliação do papel das células T CD8+ na infecção experimental por Leishmania braziliensis." reponame:Repositório Institucional da FIOCRUZ, 2011. https://www.arca.fiocruz.br/handle/icict/4200.
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Fundação Oswaldo Cruz. Centro de Pesquisas Gonçalo Moniz. Salvador, Bahia, Brasil
Linfócitos T CD8+ são células do sistema imune adaptativo capazes de induzir a morte de células infectadas através de mecanismos citotóxicos. No modelo de infecção intradérmica por Leishmania revelou-se que os linfócitos T CD8+ são responsáveis tanto pela indução de patogênese bem como pela imunidade contra a infecção primária por L. major. Até o momento, o papel dos linfócitos T CD8+ não foi estudado na infecção experimental por L. braziliensis. Neste estudo, investigamos o recrutamento dos linfócitos T CD8+ para o sítio de infecção e determinamos a sua função. Cinco semanas após a infecção intradérmica por L. braziliensis, camundongos BALB/c apresentaram um aumento na porcentagem de linfócitos T CD8+ presentes na orelha infectada e estes produziram, principalmente, IFN-g e Granzima B. Já no linfonodo de drenagem, estas células não produzem granzima mas, sim, IFN-g e TNF-a. Utilizando o mesmo modelo de infecção, camundongos BALB/c ou C57BL/6 depletados de linfócitos T CD8+ ou camundongos deficientes em b2-microglobulina ou em CD8 apresentaram redução no tamanho da lesão ao longo da infecção e menor carga parasitária cinco semanas após a infecção. A depleção de linfócitos T CD8+ não induziu qualquer alteração no recrutamento e produção de IFN-g, TNF-a e IL-10 pelos linfócitos T CD4+ no sítio de infecção ou no linfonodo de drenagem. Além disso, a capacidade proliferativa ou a produção de citocinas específicas in vitro após estímulo com células dendríticas infectadas por L. braziliensis não sofreram alteração. A ausência de linfócitos T CD8+ após a 8 infecção por L. braziliensis também não alterou o recrutamento de monócitos inflamatórios nem a sua diferenciação em células dendríticas. Por último, a análise histológica e de citometria de fluxo mostrou aumento no recrutamento de neutrófilos para o sítio de infecção e este resultado pode ser correlacionado com o controle da doença. Para confirmar o envolvimento dos linfócitos T CD8+ no desenvolvimento de lesão por L. braziliensis, transferimos linfócitos T CD8+ de camundongos naïve ou imunes, bem como linfócitos T CD4+ somente ou linfócitos T CD8+ e T CD4+ para camundongos RAG-/-. Neste contexto, a transferência de linfócitos T CD8+ naïve ou imunes induziu uma intensa patologia no sítio de infecção bem como a disseminação de parasitas para outros sítios, como a orelha não infectada, pata e nariz. Camundongos RAG-/- controle e aqueles que receberam linfócitos T CD8+ naïve ou imunes apresentam a mesma quantidade de parasitas no sítio de infecção, embora o aspecto da lesão tenha sido muito diferente. A transferência de linfócitos T CD4+ foi capaz de controlar a carga parasitária nestes animais e o mesmo foi observado após transferência de linfócitos T CD4+ e T CD8+ em conjunto. Nestes animais não observamos lesões em outros sítios, indicando que os linfócitos T CD8+ contribuem para a disseminação dos parasitas. Por último, transferimos linfócitos T CD8+ provenientes de camundongos selvagens ou deficientes de IFN-g e perforina e observamos que, na ausência de perforina, a patologia e a disseminação parasitária são controladas. Portanto, este estudo sugere envolvimento dos linfócitos T CD8+ na patogênese induzida por L. braziliensis devido ao seu potencial citotóxico e, em paralelo, inibindo o recrutamento de neutrófilos para o sítio de infecção.
CD8+ T lymphocytes are part of the adaptive immune system and are considered cytotoxic because of their ability to induce death in infected cells. Using the intradermal model of Leishmania infection, it has been shown that CD8+ T cells play an essential role in both pathogenesis and immunity to primary infection with L. major in the skin. So far, the role of these lymphocytes in the experimental model of infection using L. braziliensis has not been evaluated. In this study we determined the recruitment and function of these cells upon infection with L. braziliensis. Five weeks after infection, the frequency of CD8+ T cells was increased in the dermal site and these cells produced mainly IFN-g and granzyme B in infected mice. In the draining lymph nodes, these cells produced high levels of IFN-g and TNF-a, but not granzyme B. Using the same intradermal model of infection, we analysed the outcome of infection in the absence of CD8+ T lymphocytes using both antibody depletion in BALB/c and C57BL/6 mice and mice deficient in b2- microglobulin and CD8. In all groups, the absence of CD8+ T cells was correlated with better control of lesion development and parasite load in both depleted BALB/c and in b2-microglobulin deficient mice. In the absence of CD8+ T cells, CD4+ T lymphocytes were recruited to the same extension and produced same levels of IFN-g, TNF-a and IL-10 both in the infected ear and in draining lymph nodes when compared to infected mice that were not depleted. Also, there was no change in the proliferative potential and in IFN-g production by these cells after re-stimulation with infected dendritic cells. Analysis of inflammatory monocyte recruitment and differentiation of these cells into dendritic cells were similar in both depleted and non-depleted mice. On the other hand, histological and flow cytometric analyses showed increased neutrophil recruitment to the site of infection and this can be correlated with disease control. To confirm the role of CD8+ T cells in the lesion development of L. braziliensis infected mice, we then transferred CD8+ T cells from naïve or immune mice, as well as CD4+ T cells alone or together with T CD8+ to RAG deficient mice. The transfer of CD8+ T cells from immune or naïve mice into RAG recipients induced an intense pathology upon infection with L. braziliensis in the infection site, but also in uninfected tissues such as the uninfected ear, nose and footpad. Evaluation of parasite numbers in the infected ear showed that RAG deficient mice without T cells and those transferred with CD8+ T cells from naïve or immune mice had similar number of parasites although the pathology was very different. The transfer of CD4+ T cells alone or in association with CD8+ T cells induced parasite control in the infection site. In these mice, we could not detect lesions in other sites and we concluded that the transfer of CD8+ T cells alone induces parasite dissemination in RAG deficient mice. Finally, the transfer of CD8+ T cells from perforin deficient mice led to control in lesion development and in parasite dissemination. In this study we can conclude that CD8+ T cells are involved in the pathogenesis of L. braziliensis due to their cytotoxic potential and by inhibiting neutrophil recruitment to the infection site.
Herrmann, Alexander Michael [Verfasser], and Heinz [Gutachter] Wiendl. "CD8+ Lymphozyten mediierter Angriff auf Neuronen des ZNS: Relevanz von Granzym B und Perforin für akute elektrophysiologische Veränderungen / Alexander Michael Herrmann. Gutachter: Heinz Wiendl." Würzburg : Universität Würzburg, 2015. http://d-nb.info/1108781152/34.
Full textSumaria, Nital. "The relevance of specific molecular and cellular effectors during murine cytomegalovirus infection." University of Western Australia. School of Biomedical, Biomolecular and Chemical Sciences, 2008. http://theses.library.uwa.edu.au/adt-WU2008.0116.
Full textMusembi, Susan Mbithe. "Immunological assays relevant to definition of bovine theileria parva-specific cytotoxic CD8+ T cell responses." Thesis, Brunel University, 2012. http://bura.brunel.ac.uk/handle/2438/7171.
Full textAugustin, M. (Merja). "Cytotoxic lymphocytes in children's cow's milk sensitive enteropathy of delayed type." Doctoral thesis, University of Oulu, 2005. http://urn.fi/urn:isbn:9514277244.
Full textMasouris, Ilias [Verfasser], and Elfriede [Akademischer Betreuer] Nößner. "Verteilung und zytotoxische Qualität von T-Zellen und natürlichen Killerzellen im klarzelligen Nierenzellkarzinom : Gefäßsystem-bezogene Lokalisation und Ausstattung mit Perforin beeinflussen Metastasierung und Tumor-spezifisches Überleben / Ilias Masouris. Betreuer: Elfriede Nößner." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2016. http://d-nb.info/1084582740/34.
Full textFauteux-Daniel, Sébastien. "Étude du rôle de l’inflammasome et de la kinase Styk1 dans la régulation des lymphocytes cytotoxiques." Thesis, Lyon, 2018. http://www.theses.fr/2018LYSE1052/document.
Full textUpon recognition of infected or target cells, CD8+ T and Natural Killer (NK) lymphocytes initiate a polarized degranulation of vesicle storing cytotoxic molecules (perforin: PRF1 and granzyme B). By altering the target cell’s cellular membrane integrity, perforine allows granzyme B to translocate to its cytosol. Genetic anomalies may affect normal cytotoxic functions and severely hamper the control of intracellular pathogens. In this context, the pathogenic signal remains uninterrupted and both cytotoxic lymphocytes and macrophages are continuously stimulated. This auto-inflammatory pathological condition is named hemophagocytic lymphohistiocytosis (HLH) and is fatal without therapeutic intervention. HLH can also occur secondary to infection with viruses from the herpesviridae family, or be concomitant to important immune alterations such as systemic onset juvenile idiopathic arthritis (SoJIA), with no clear etiological cause identified. In 2014, a case of HLH mediated by the constitutive activation of the NLRC4 inflammasome receptor was first described. The inflammasome is a multimeric structure involving a cytosolic receptor, a scaffold protein – ASC – and Caspase-1. In the immune system, the inflammasome is expressed in macrophages and dendritic cells and senses pathogenic (PAMP) and danger (DAMP) associated signals. Once activated, inflammasome’s protein Caspase-1 catalyzes the maturation of pro-IL-1b and pro-IL-18 and leads to their secretion. Since NLRC4 constitutive activation appears to be sufficient for triggering HLH, we aimed to understand if the inflammasome structure was essential to the development of the syndrome. In order to address this question, we invalidated the inflammasome through the abrogation of ASC or Caspase-1 in PRF1 -/- HLH mouse model. We also tested the hypothesis that an altered cytotoxic function could explain the high prevalence of HLH in the proinflammatory context of SoJIA. The results we present here show that the inflammasome is responsible for the elevated levels of IL-18 in the serum of HLH patients. However, the inflammasome is facultative for its development. We also demonstrate that in patients suffering from SoJIA, NK cells show normal cytotoxicity, suggesting that immunological mechanisms involved in FHL and secondary HLH are distinct. In the second part of this manuscript, we aim at understanding the role of Styk1 serine/threonine/tyrosine kinase in NK cells’ regulation. NK cells are in charge of eliminating stressed, virally infected or transformed cells. Upon activation, they secrete large amounts of IFN-γ and TNF-α, thus bridging innate and adaptive immunity. Capabilities for recognition of target cells is endowed by the expression of numerous stochastically expressed activating and inhibitory receptors. The balance between activating and inhibitory signal allows for self-tolerance or activation upon engagement of abnormal cells. Activating and inhibitory receptor are germline encoded in two dense, large complexes, the Natural Killer Complex (NKC) and the Leukocyte Receptor Complex (LRC). At the moment of starting this work, we had recently identified that Styk1 was a signature transcript of NK cells. However, its function in NK cells and more generally in the immune system remains unknown. Nevertheless, its genetic localisation near the NKC and its potential implication in the PI3K-AKT pathway prompt that it may play a role in NK cell development and/or functions. In order to evaluate the role of Styk1 in NK cells’ regulation, we generated a mouse model in which its expression is abrogated. Our data confirms that amongst all immune subsets, Styk1 is specifically expressed by NK cells. Styk1 was also able to discriminate NK cells from other ILCs. In this study, we show that Styk1 invalidation lead to a decrease of activity in the AKT/mTOR pathway. However, NK cells development, homeostasis and function were surprisingly normal in Styk1 -/- mice
Sleater, Michelle Leigh. "Cellular and molecular effector mechanisms of islet allograft rejection /." Connect to full text via ProQuest. IP filtered, 2006.
Find full textTypescript. Includes bibliographical references (leaves 151-168). Free to UCDHSC affiliates. Online version available via ProQuest Digital Dissertations;
Wang, Xisheng. "Mechanisms of IFN-gamma-mediated Resistance against Development of Toxoplasmic Encephalitis." Diss., Virginia Tech, 2006. http://hdl.handle.net/10919/30268.
Full textPh. D.
Talbot-Honeck, Carole. "Excellence in the performing arts: A study of elite musicians' mental readiness to perform." Thesis, University of Ottawa (Canada), 1994. http://hdl.handle.net/10393/10348.
Full textVasireddi, Mugdha. "Subversion of Natural Killer Cell Defenses Induced by a Deadly Zoonotic Virus." Digital Archive @ GSU, 2009. http://digitalarchive.gsu.edu/biology_diss/65.
Full textKinney, Daryl Wayne. "The Effect of School Performing Ensemble Participation on the Ability to Perform and Perceive Expression in Music." The Ohio State University, 2001. http://rave.ohiolink.edu/etdc/view?acc_num=osu1392813859.
Full textAndrews, Stuart L. "Performing histories : the politics of performing the past." Thesis, Lancaster University, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.420696.
Full textKelly, Traci. "Performing Intersubjectivity." Thesis, University of Reading, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.525121.
Full textCornea, Christine. "Performing cyborgs." Thesis, University of Southampton, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.364752.
Full textReynoso, Humberto. "Performing Binaries." CSUSB ScholarWorks, 2015. https://scholarworks.lib.csusb.edu/etd/252.
Full textFine, Jenny. "Performing Tenderness." The Ohio State University, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=osu1276799884.
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Full textAvailable via ProQuest Digital Dissertations. Vita. Includes bibliographical references (p. 239-249).