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Dissertations / Theses on the topic 'Cellular immunity'

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Published: 4 June 2021
Last updated: 28 July 2024

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1

Shimokata, Kaoru. "Cytokines and Local Cellular Immunity." 名古屋大学医学部, 1997. http://hdl.handle.net/2237/6185.

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2

Wuttge, Dirk Marcus. "Cellular immunity and inflammation in atherosclerosis /." Stockholm : Karolinska Univ. Press, 2001. http://diss.kib.ki.se/2001/91-7349-051-2/.

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3

Yassine, Daadaa. "Network Decontamination with Temporal Immunity." Thèse, Université d'Ottawa / University of Ottawa, 2012. http://hdl.handle.net/10393/20633.

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Network decontamination is a well known mobile agent problem with many applications. We assume that all nodes of a network are contaminated (e.g., by a virus) and a set of agents is deployed to decontaminate them. An agent passing by a node decontaminates it, however a decontaminated node can be recontaminated if any of its neighbours is contaminated. In the vast literature a variety of models are considered and different assumptions are made on the power of the agents. In this thesis we study variation of the decontamination problem in mesh and tori topologies, under the assumption that when a node is decontaminated, it is immune to recontamination for a predefined amount of time t (called immunity time). After the immunity time is elapsed, recontamination can occur. We focus on three different models: mobile agents (MA), cellular automata (CA), and mobile cellular automata (MCA). The first two models are commonly studied and employed in several other contexts, the third model is introduced in this thesis for the first time. In each model we study the temporal decontamination problem (adapted to the particular setting) under a variety of assumptions on the capabilities of the decontaminating elements (agents for MA and MCA, decontaminating cells for CA). Some of the parameters we consider in this study are: visibility of the active elements, their ability to make copies of themselves, their ability to communicate, and the possibility to remember their past actions (memory). We describe several solutions in the various scenarios and we analyze their complexity. Efficiency is evaluated slightly differently in each model, but essentially the effort is in the minimization of the number of simultaneous decontaminating elements active in the system while performing the decontamination with a given immunity time.
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4

Makedonas, George. "Cellular immunity among HIV exposed, uninfected individuals." Thesis, McGill University, 2005. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=111828.

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Two models of HIV infection have been studied extensively with the goal of identifying immune correlate(s) of protection against HIV: (1) the simian immunodeficiency virus (SIV) infection of rhesus macaque monkeys and (2) individuals with repeated exposure to HIV who remain uninfected by the virus (EUs). Both paradigms suggest that T cell-mediated immunity plays an important role in controlling HIV replication. Evidence from the SIV/macaque system, however, predicts that HIV vaccines aimed at eliciting T cell responses will fail to induce sterilizing immunity against HIV. The aim of the work presented in this thesis was to correlate HIV-specific T cell immunity in EUs with protection from HIV infection. The study cohort was comprised of (a) men who have unprotected sexual intercourse with HIV-infected men (MSM), (b) intravenous drug users (IVDU) who share syringes with HIV-infected peers, and (c) heterosexual partners of HIV-infected subjects. EUs were shown to exhibit HIV-specific IFN-gamma secretion, IL-2 production, and T cell proliferation, whereas low-risk negative controls did not. Furthermore, HIV-specific IFN-gamma secretion and T cell proliferation were not observed among a population of EUs who seroconverted soon after the tested time point. HIV-specific IL-2 secretion and T cell proliferation were shown to be correlated in our cohort of EUs. These effector functions are considered hallmark properties of central memory T cells (TCM), the subset of memory T cells that has been shown to mediate sterilizing immunity in mouse models of viral infection. The presence of TCM in EUs implies the development of immunity against HIV that is either fully protective or partially so, by increasing the threshold for HIV infection. Since these HIV-specific effector functions were absent in EUs who eventually seroconverted, it can be inferred that EUs in our cohort develop HIV-specific T cell immunity that mediates protection from HIV infection. Thus, our contribution to the EU paradigm is that sterilizing immunity is an attainable goal of prospective HIV vaccines.
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5

Tye, Gee Jun. "Combined adjuvant for stimulation of cellular immunity." Thesis, King's College London (University of London), 2012. https://kclpure.kcl.ac.uk/portal/en/theses/combined-adjuvant-for-stimulation-of-cellular-immunity(b1be07ae-b8d4-40a8-9258-bc3e3413df9d).html.

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Vaccination has important clinical potential in the immunotherapy of both infectious disease and cancer. The central aim of the studies reported in this thesis has been the development of vaccination strategies that will be effective for therapeutic applications in cancer. Using ovalbumin antigen in a mouse model, we have examined a combination of recently developed adjuvants referred to as CASAC (combined adjuvants for synergistic stimulation of cellular immunity) to optimise the efficacy of vaccination induced T cell mediated immunity. These studies have examined the effect of repeated rounds of vaccination with one, or alternating cycles of two different helper peptides. The hypothesis was that repeated stimulation of the same clonal population of CD4+ T helper cells with a single MHC class II peptide could induce anergy, exhaustion, clonal deletion and/or stimulation of regulatory T-cells, resulting in reduced and shorter lived immunity. These studies have also examined the effect of inclusion of other immune regulatory components, and in particular a cocktail of cytokines generated by phytohemagglutinin stimulation of human peripheral blood mononuclear cells (referred to as IRX-2). Another important issue for vaccination mediated immune therapy that was addressed is the age-associated loss of immunological competence (immunesenescence). A comparative analysis is reported of the magnitude and duration of responses to vaccination with a single MHC class-I presented peptide in combination with the same or alternating MHC class-II presented peptides. In addition, we have quantified the number of antigen specific CDS T cells, their effector and memory subsets and in vivo antigen specific cytolytic activity to examine the effect of CASAC vaccination alone or in combination with IRX-2. The induction of immunological responses in young and aged immune backgrounds was also examined. Vaccinations with ovalbumin peptides in the CASAC adjuvant have shown higher percentages and numbers of antigen specific CDS T cells with improved cytolytic activity when helper functions are stimulated by two different class-II peptides used in alternating cycles of vaccination, rather than repeated stimulation by the same class-II peptide. This conclusion can be confirmed with a repeated experiment. Analysis of T cells with a regulatory (Treg) phenotype (CD4+CD25+Foxp3+) showed that their expansion was reduced with the alternating T-helper peptide vaccination regimen. The addition of IRX-2 to the CASAC vaccination regimen was found to enhance the in vivo antigen specific cytolytic activity. This was particularly significant in the aged mice which were found to have increased levels of Tregs.
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6

Patel, Mihil. "Regulation of cellular immunity by human cytomegalovirus." Thesis, Cardiff University, 2018. http://orca.cf.ac.uk/114496/.

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The success of HCMV as a lifelong pathogen is attributed at least in part to the broad range of encoded immune evasion molecules that inhibit the host cellular immune response. Indeed, HCMV has become a paradigm for immune evasion, the study of which has revealed a number of basic immunological processes. To screen for novel immune evasion genes, HCMV-specific CD8+ T-cell lines were grown from seropositive donors and used against a series of block deletion viruses, each missing a region of genes non-essential for replication in vitro. UL13-UL20 was flagged as important for inhibition of CD8+ T-cells. Further screening with individual gene knockout HCMVs showed that the published NK-cell inhibitor UL16 could inhibit CD8+ T-cells, but also revealed UL19 as a previously unrecognised strong immune evasin, inhibiting 3 separate CD8+ T-cell lines. UL19 had no effect on HLA-I downregulation indicating that it may affect other pathways involved with T-cell activation. Proteomic data showed that surface TNFR2 was increased by HCMV infection. This is important as this would influence the response to TNF, a major inflammatory cytokine and soluble effector molecule released by T and NK cells. Screening using different HCMV strains and knockout viruses identified UL148 and UL148D as responsible for the increase in surface TNFR2 but prevented the release of soluble TNFR2, indicating that UL148 and UL148D were influencing the ability of TNFR2 to be retained at the cell surface. Infection with HCMV Merlin profoundly downregulated surface ADAM17, the metalloproteinase responsible for cleaving TNFR2 from the cell surface. Deleting UL148 and UL148D recovered ADAM17 expression, blocking the function of which returned surface and soluble TNFR2 levels to those observed with Merlin. This was also true of TNFR1. HCMV infected cell lysates showed that UL148 and UL148D interfered with the maturation of ADAM17. Thus, UL148 and UL148D allow upregulation of TNFR2 and maintain TNFR1 expression during and HCMV infection by impairing surface ADAM17 expression through impairment of ADAM17 maturation. Given that ADAM17 is involved with the cleaving of multiple cytokines, cytokine receptors, adhesion molecules and immune cell receptors, this work identifies a novel mechanism through which HCMV can alter the surface and soluble proteome by preventing the shedding of inflammatory/immune receptors and mediators. More detailed studies will be required to define the global impact of this on the immune system.
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7

Abuhammash, E. V. "Transfer actor as mediator of cellular immunity." Thesis, Сумський державний університет, 2013. http://essuir.sumdu.edu.ua/handle/123456789/32144.

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Transfer factor (s) - are small molecules, that transfer the ability to recognize pathogens (bacterial or viral) cells of the immune system, never exposed to this pathogen. When you are citing the document, use the following link http://essuir.sumdu.edu.ua/handle/123456789/32144
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8

Oldenhove, Guillaume. "Contrôle de la réponse immunitaire induite par les cellules dendritiques: rôle des cellules T régulatrices naturelles ou induites." Doctoral thesis, Universite Libre de Bruxelles, 2006. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/210888.

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9

Weber, Wilhelm Evert Jacob. "Cellular auto-immunity in central nervous system disease." Maastricht : Maastricht : Rijksuniversiteit Limburg ; University Library, Maastricht University [Host], 1988. http://arno.unimaas.nl/show.cgi?fid=5594.

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10

Nickless, Jane Christina. "Cellular immunity to acetylcholine receptor in myasthenia gravis." Thesis, University of Bath, 1985. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.767550.

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Nicotinic acetylcholine receptor (AChR) has been purified from Torpedo electric organ, foetal calf muscle, adult human leg muscle, and foetal human skeletal muscle, by extraction in non-ionic detergent followed by affinity purification on immobilised a-toxin. The purified AChR preparations were used to study cellular responses in vitro from patients with myasthenia gravis. In addition, several characterisation studies were carried out on the foetal calf AChR preparation. Purified foetal calf AChR was shown in isoelectric focussing experiments to focus as a single sharp peak at pH 5.2 +/- 0.1, and the receptor sedimented in sucrose density gradients as a single species with a sedimentation coefficient S20w= 9.35 +/- 0.10 S, when indirectly labelled with [125 I]-a-bungarotoxin. SDS-polyacrylamide gel electrophoresis of purified foetal calf AChR consistently showed five major protein bands with (Mr) 40, 44, 47, 52 and 57 K. The 57K protein sub-unit was always the most prominent band. A procedure by which to measure antigen-specific lymphocyte proliferation in vitro was developed and optimised in a system using tetanus toxoid and peripheral blood mononuclear leucocytes (PBL) from a normal donor recently immunised against tetanus. Conditions for the production of human T-cell growth factor (TCGF), or Interleukin 2 (IL-2) were optimised, and used in the tetanus toxoid system to develop a procedure by which antigen-specific reactive T-lymphocytes could be isolated, expanded into long-term lines, and ultimately cloned. Antigen and TCGF were required for the expansion and maintenance of the T-cell lines and clones. The AChR purification procedure was modified several times in order to obtain a workable, non-inhibitory AChR preparation for studies of myasthenia gravis in vitro. Lymphocytes, collected from myasthenic blood samples, were shown to proliferate weakly in response to purified AChR added in vitro, with a mean stimulation index (+/- SEM) of 1.72 +/- 0.12. The proliferative response did not appear to be related to the species of AChR employed, age, sex, or clinical classification of the patient, but higher stimulation indices were obtained from patients in a state of disease exacerbation at the time the sample was taken. T-cell fractionation, or reactive T-cell pre-selection steps, did not enhance the proliferative response of myasthenic lymphocytes to purified AChR in vitro, and attempts to isolate and expand AChR-autoreactive T-lymphocytes using antigen and IL-2 were unsuccessful.
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11

Watkins, Marcia Linda Vivienne. "Cellular immunity of naïve and BCG vaccinated neonates." Doctoral thesis, University of Cape Town, 2010. http://hdl.handle.net/11427/10984.

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Includes abstract.
Includes bibliographical references (leaves 153-187).
Despite more than 95% vaccination coverage with Mycobacterium bovis Bacille Calmette-Guérin (BCG), tuberculosis (TB) remains epidemic in South Africa. The dichotomy that successful pregnancy is usually associated with a type 2 (Th2) cytokine profile in the newborn child, whereas immunity to Mycobacterium tuberculosis (Mtb) is associated with the development of a type 1 helper (Th1) cytokine response, could impact on the subsequent adaptive immune response to BCG vaccination. Previous studies have suggested that immune responses in early life may be defective and related to the immaturity of antigen-presenting cells and/or T cells.
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12

Zettervall, Carl-Johan. "Signaling pathways in the activation and proliferation of Drosophila melanogaster blood cells." Doctoral thesis, Umeå : Umeå centrum för molekylär patogenes (UCMP), 2005. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-513.

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13

Haque, Khawaja Mostaq Gausul. "The quantitation of cellular allo-immunity in preparation for monitoring of cellular tolerance." Thesis, University of Bristol, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.389232.

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14

Mäkitalo, Barbro. "HIV and SIV specific cellular immunity in macaque models /." Stockholm, 2003. http://diss.kib.ki.se/2003/91-7349-751-7/.

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15

Struik, Siske Sybrich. "Cellular immune responses and clinical immunity to P. falciparium." Thesis, London School of Hygiene and Tropical Medicine (University of London), 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.417697.

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16

McLarnon, Andrew. "Cellular mechanisms of alloreactive immunity following stem cell transplantation." Thesis, University of Birmingham, 2011. http://etheses.bham.ac.uk//id/eprint/3064/.

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Allogeneic stem cell transplantation is associated with a powerful T cell-mediated ‘graft-versus-leukaemia’ (GvL) effect and also ‘graft-versus-host disease’ (GvHD). Developing therapies to improve survival relies on greater understanding of these responses in order to enhance GvL and suppress GvHD. To gain an increased understanding of the mechanisms of GvHD I measured frequencies of Th1, Th17 and Treg subsets in the blood of 32 GvHD patients (during and outside of disease episodes) and in 21 patients who did not suffer GvHD. No associations between T cell subset frequencies or serum cytokine concentrations and incidence of GvHD were evident. My GvL work addressed whether T cell responses to cancer/testis antigens (CTAg) could be detected in a cohort of 41 patients who had undergone allogeneic stem cell transplantation for the management of acute myeloid leukaemia and multiple myeloma. CTAg-specific CD8+ T cell immune responses were observed within peripheral blood of five patients, with an average magnitude of 0.045% of the CD8+ T cell repertoire. T cell immunity was focussed against peptides derived from MAGE proteins and was increased within the bone marrow. These immune responses are likely to contribute to tumour eradication following transplantation and represent a potential novel mechanism for GvL.
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17

Marques, Mariana Campos. "Cellular responses to viral infection : proteostasis and innate immunity." Master's thesis, Universidade de Aveiro, 2017. http://hdl.handle.net/10773/22054.

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Mestrado em Biomedicina Molecular
Viruses are small opportunistic infectious agents. Virus entry, replication and assembly are dynamic and coordinated processes that require precise interactions with host components, often with cellular organelles. Hence, we proposed to study two different viruses affecting two distinct cellular surveillance mechanisms: Human Cytomegalovirus (HCMV) and Influenza A Virus (IAV) influence on the innate immune response and proteostasis, respectively. HCMV might be associated with additional long-term health consequences in human due to its ability to establish a lifelong persistent latent infection. HCMV encodes vMIA, an anti-apoptotic protein known to co-localize at peroxisomes and mitochondria, induce their fragmentation and inhibit the downstream cellular antiviral response that is established at both organelles. In the present work, we aimed to characterize the role of vMIA in the peroxisomal-MAVS dependent antiviral response. We proposed to map the vMIA domains responsible for the organelles’ morphology changes and innate immune response inhibition. Our results revealed that the 115-130 amino acid sequence might be important for the organelles’ fragmentation. We also found that m38.5, an analogue of vMIA in murine CMV (MCMV) seems to localize at peroxisomes, induce the organelle’s fragmentation and clearly inhibit the peroxisome-dependent antiviral immune response. These results suggest that this virus may be useful to complement our results with experiments performed in animals or in the context of a viral infection. IAV is the causative agent for most of the annual epidemic in humans. During IAV infection, it occurs the accumulation of unfolded proteins and the formation of specialized sites of viral replication, resulting in the formation of insoluble aggregates or inclusions. In this study, we proposed to determine whether and how IAV infection leads to aggresomal-prone proteins accumulation. Our preliminary results suggest aggresomes formation during viral infection, previous to the vRNP release in to the cytoplasm.
Os vírus são agentes infeciosos oportunistas. Os diferentes passos de um ciclo de vida viral, incluindo a entrada do vírus na célula, a replicação do seu genoma e a formação de novas partículas virais requerem interações com os diferentes componentes celulares do hospedeiro, nomeadamente com organelos. Neste projeto, propomos estudar dois tipos diferentes de vírus que afetam dois mecanismos distintos de sobrevivência celular: a influência do Citomegalovírus de humano (HCMV) na resposta imunitária inata e o efeito do Vírus da Influenza A (IAV) na proteostase. O HCMV pode estar associado com consequências graves para a saúde da população, uma vez que tem a capacidade para estabelecer uma infeção latente e persistente no hospedeiro. Este vírus codifica para a vMIA, uma proteína anti-apoptótica que se localiza nos peroxissomas e nas mitocôndrias, induzindo a sua fragmentação e inibindo a resposta antiviral celular que é estabelecida em ambos. Com isto, sugerimos mapear os domínios da vMIA responsáveis pelas alterações na morfologia dos organelos e na inibição da resposta imune. Os nossos resultados revelaram que a sequência de aminoácidos 115-130 poderá ser importante para a fragmentação dos organelos. Também descobrimos que a proteína m38.5 do Citomegalovírus de ratinho (MCMV), análoga à vMIA, parece localizar nos peroxissomas, induzir a sua fragmentação e claramente inibir a resposta antiviral dependente deste organelo. Estes resultados sugerem que este vírus poderá ser útil para complementar os nossos resultados com experiências animais ou no contexto de infeção viral. O IAV é o agente causativo da maioria das epidemias anuais em humanos. Durante a infeção com IAV, ocorre acumulação de proteínas com conformação errada e a formação de locais especializados de replicação viral, resultando na formação de agregados insolúveis ou inclusões. Neste estudo, propusemos determinar se a infeção com IAV conduz à acumulação de proteína com pré-disponibilidade para formar agressomas. Os nossos resultados, embora preliminares, sugerem que existe formação destas estruturas durante a infeção viral, previamente à libertação do genoma viral no citoplasma.
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Noble, Roger Lee. "Cellular Immunity in Children with Down Syndrome (Trisomy-21)." DigitalCommons@USU, 1985. https://digitalcommons.usu.edu/etd/4640.

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Individuals with Down syndrome (US) suffer from increased incidence of respiratory infections and lymphoblastic leukemia, and a death rate that is particularly high in the first 5 years of life. Relatively few studies have probed immune parameters in young US children. Primary immune defects in DS may be masked by a degree of immune maturity in adults, and hygienic factors may have an effect on immune capability throughout the years. A study of young children can give clearer evidence of the actual primary immune defects in DS. Blood samples were drawn from 20 DS children under 6 years old and from age-matched controls. Packed blood cell volume was measured, various blood cell subpopulations were enumerated and differential counts were performed. Several tests of cellular immune function were performed and plasma zinc levels were determined using atomic adsorption spectrophotometry. Elevated hematocrit levels were observed in the US group. White blood cell counts and proportions of rosette-forming cells were normal in blood from DS children. Altered neutrophil and lymphocyte proportions in DS samples resulted from a depressed number of circulating lymphocytes in the these subjects. This indicated that T cell numbers are low in DS. DS individuals had a low number of circulating OKT4+ T cells which resulted in significantly depressed T4:T8 ratios. Cells from DS subjects exhibited a reduced proliferative response to phytohemagglutinin; a low response to the optimal concentration of concanavalin A was seen with DS samples, but at suboptimal doses the response was normal; suboptimal concentrations of pokeweed mitogen elicited normal responses by cells from DS children. Preliminary results suggest that interleukin-2 (IL-2) production in young children may correlate positively with age and that DS subjects may produce normal or elevated amounts of IL-2. This suggests that IL-2 receptor function may be defective in T cells from DS children. DS children had normal natural killer cell activity and cells from those children were no more sensitive to the augmenting effects of interferon-alpha than cells from control children. Plasma zinc levels in DS appeared to be normal. These findings not only provide evidence that the primary immune defect in DS involves low levels of T cells, but they show depressed number and function of helper T cells and suggest defective IL-2 receptor expression in DS.
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Temmerman, Stéphane. "Etude de la réponse à médiation cellulaire indute par l'héparin-binding hemagglutinin chez le sujet infecté par Mycobacterium tuberculosis." Doctoral thesis, Universite Libre de Bruxelles, 2004. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/211117.

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La tuberculose demeure un problème majeur de santé publique. Mycobacterium tuberculosis infecte un tiers de la population mondiale et environ 3 millions de décès, des suites de l’infection, sont recensés chaque année dans le monde. La mise au point d’une stratégie vaccinale efficace constitue dès lors la solution idéale pour tenter d’éradiquer la bactérie. Le système immunitaire humain répond à l’infection par l’induction d’une réponse cellulaire, caractérisée essentiellement par la sécrétion de médiateurs pro-inflammatoires, comme l’interféron-gamma (IFN-?). A la fois les lymphocytes T CD4+ et T CD8+ produisent cette cytokine, mais les seconds sont également doués de propriétés cytotoxiques, entraînant la mort de la cellule infectée et du bacille. L’évaluation du potentiel de nouveaux candidats vaccins implique dès lors la caractérisation exhaustive de la réponse immunitaire induite.

La « heparin-binding hemagglutinin (HBHA) » est une protéine de 28-kDa, sécrétée et exprimée à la surface de M. tuberculosis et de M. bovis BCG. Montrant une affinité importante pour les gycoconjugués sulfatés, elle favorise la dissémination hématogène du bacille de Koch.

Nos résultats démontrent que la HBHA stimule l’immunité à médiation cellulaire humaine avec, toutefois, des différences selon que le sujet infecté souffre ou non de tuberculose active. En effet, les cellules mononuclées circulantes, de la majorité des individus infectés mais non-malades, secrètent de l’IFN-? en réponse à la HBHA, alors qu’une minorité de sujets malades produit de faibles quantités d’IFN-? après stimulation in vitro avec l’antigène. Lors de l’infection naturelle par le bacille de Koch, la HBHA devient dès lors une cible pour le système immunitaire, et plus particulièrement au sein des sujets, généralement considérés, comme protégés.

L’analyse de la réponse cellulaire, spécifique à l’adhésine, démontre que les lymphocytes T CD4+, mais également T CD8+, des sujets infectés mais non-malades, produisent de l’IFN-? L’antigène est effectivement présenté aux lymphocytes T grâce aux glycoprotéines du complexe majeur d’histocompatibilité de classe I et de classe II. Le phénotypage des cellules productrices d’IFN-? témoigne également la participation des cellules « natural killer (NK) » dans la réponse immunitaire contre la HBHA. En l’absence des lymphocytes T restreints à l’antigène, les cellules NK se montrent toutefois incapables de secréter de l’IFN-? au contact de la HBHA. Les interactions entre les lymphocytes T, spécifiques à l’antigène, déterminent également la production de cytokines. Alors que la déplétion des cellules T CD8+ diminue légèrement la production d’IFN-? l’absence des lymphocytes T CD4+ abolit toute sécrétion résiduelle d’IFN-? lors de la stimulation avec la HBHA. Par contre, les lymphocytes T CD8+, pré-stimulés avec l’antigène en présence de cellules T CD4+, répondent secondairement à la présentation de la HBHA par des macrophages. Ce résultat suggère une coopération entre ces deux sous-populations cellulaires, afin de produire de l’IFN-? à l’encontre de la HBHA. Grâce à un contact cellulaire, les lymphocytes T CD4+ spécifiques à la HBHA soutiennent effectivement l’activation des cellules T CD8+.

Outre la production de cytokines, la participation des lymphocytes T CD8+ à la lutte contre M. tuberculosis, se traduit également par leurs fonctions cytotoxique et bactéricide. La caractérisation des cellules T CD8+, spécifiques à la HBHA, s’est dès lors poursuivie par l’évaluation de leur potentiel cytolytique. Après expansion clonale, les lymphocytes T CD8+ induisent la mort des macrophages présentant la HBHA. Le mécanisme cytotoxique engage la libération du contenu des granules cytoplasmiques, comme le montre l’augmentation de la synthèse de perforine et de granzyme A, lorsque les cellules T CD8+ sont stimulées avec la HBHA. Privés de ces médiateurs solubles, les lymphocytes T CD8+, spécifiques à la HBHA sont alors incapables de lyser les cellules cibles. En définitive, l’activité microbicide constitue actuellement le meilleur corrélat de protection. La culture de macrophages infectés par M. bovis BCG, en présence de cellules T CD8+ spécifiques à la HBHA, limite partiellement la croissance de la bactérie phagocytée, soulignant le pouvoir anti-mycobactérien de l’immunité cellulaire induite par la HBHA, chez le sujet infecté mais non-malade.

D’autre part, l’analyse biochimique, menée à l’Institut Pasteur de Lille, démontre que la HBHA subit une modification post-traductionnelle, lors de sa synthèse. Il s’agit d’une méthylation des multiples résidus lysine, qui composent son extrémité C-terminale. La comparaison des formes native méthylée et recombinante non-méthylée de la HBHA démontre que la méthylation détermine l’immunogénicité et le pouvoir protecteur de la HBHA. En effet, contrairement à la HBHA native, la forme recombinante stimule faiblement la production d’IFN-? chez les individus infectés mais non-malades, et ne protège pas la souris contre l’infection par le bacille de Koch. La sécrétion d’IFN-? est, par ailleurs, partiellement restaurée lorsque la HBHA est artificiellement méthylée in vitro. Les splénocytes murins se comportent également différemment, selon qu’ils ont été immunisés avec la forme méthylée ou non. Alors que la HBHA recombinante est immunogène chez la souris et chez l’homme, l’immunité cellulaire murine induite demeure impassible face à l’infection des phagocytes par les mycobactéries, ce qui se traduit par l’absence de protection.

En conclusion, la HBHA se compose d’épitopes protecteurs, qui dépendent de la présence des groupements méthyls, associés à son domaine C-terminal. Il s’agit, à notre connaissance, de la première mise en évidence de l’implication de la méthylation dans la réponse d’immunité cellulaire à l’encontre d’une protéine. De plus, l’immunité adaptative spécifique à la HBHA, chez le sujet infecté mais non-malade, se caractérise par les trois principaux corrélats de protection, actuellement décrits chez l’homme. Le potentiel vaccinal de cette adhésine mycobactérienne est donc bien réel.
Doctorat en sciences biomédicales
info:eu-repo/semantics/nonPublished

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Hawke, Simon. "Cellular immunity to the human acetylcholine receptor in myasthenia gravis." Thesis, University of Oxford, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.239315.

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Coates, Christopher J. "Hemocyanin-derived phenoloxidase : biochemical and cellular investigations of innate immunity." Thesis, University of Stirling, 2012. http://hdl.handle.net/1893/12228.

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Hemocyanins (Hcs) and phenoloxidases (POs) are both members of the type-3 copper protein family, possessing di-cupric active sites which facilitate the binding of dioxygen. While Hcs and POs share a high degree of sequence homology, Hcs have been associated traditionally with oxygen transport whereas POs are catalytic proteins with a role in innate immunity. Evidence gathered in recent years details numerous immune functions for Hc, including an inducible PO activity. Unlike the pro-phenoloxidase activation cascade in arthropods, the endogenous mechanism(s) involved in the conversion of Hc into an immune enzyme is lacking in detail. The overall aim of this research was to characterise the physiological circumstances in which Hc is converted into a PO-like enzyme during immune challenge. A series of biochemical, biophysical and cellular techniques were used to assess the ability of phospholipid liposomes to mimic the well-characterised induction of PO activity in Hc by SDS micelles. Incubation of Hc purified from Limulus polyphemus, in the presence of phosphatidylserine (PS) liposomes, yielded ~ 90% of the PO activity observed upon incubation of Hc with the non-physiological activator, SDS. Phospholipid–induced PO activity in Hc was accompanied by secondary and tertiary structural changes similar to those observed in the presence of SDS. Subsequent analysis revealed that electrostatic interactions appear to be important in the PS-Hc activation complex. In vivo, PS-Hc interactions are assumed to be limited in quiescent cells. However, amebocytes undergoing apoptosis redistribute PS onto the outer leaflet of the plasma membrane, resulting in the potential for increased Hc-PS interactions. In the absence of a reliable culturing technique for L. polyphemus amebocytes, in vitro conditions were optimised for the short term maintenance of this labile cell type. Amebocytes retained viability and functionality in a medium that mimicked most-closely, the biochemical properties of L. polyphemus hemolymph. When presented with a fungal, bacterial or synthetic challenge, ~9% of amebocytes in vitro were found to be phagocytically active. Target internalisation was confirmed via the use of fluorescent quenchers and membrane probes. Within 4 hours of target internalisation, amebocytes underwent apoptosis, characterised by the loss of plasma and mitochondrial membrane potential, increased caspase-3 activity and extracellularisation of PS. Phagocytosis-induced cell death led to a proportional increase in the level of Hc-derived PO activity, suggesting that Hc may be interacting with PS present on terminal amebocyte membranes. The PO activity of Hc was investigated further in order to address an economically important issue; hyperpigmentation in commercial shellfish. While PO enzymes are thought to be the cause of hyperpigmentation in Nephrops norvegicus, evidence presented here suggests that cellular PO is inactivated after freeze-thawing, while extracellular Hc retains stability and displays a heightened level of inducible PO activity under similar treatments. Known PO inhibitors were used successfully to reduce Hc-derived PO activity, with inhibitors assumed to bind Hc in a manner similar to PO-inhibitor complexes. Structural and functional studies of hemocyanins and immune cells presented here provide new insights into the interactions of hemocyanin-activator complexes in invertebrates.
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Mackenzie, Danielle K. "Ageing and the cellular immune response in adult Drosophila melanogaster." Thesis, University of Stirling, 2014. http://hdl.handle.net/1893/20882.

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Senescence is the age-related progressive deterioration of physiological processes leading to an increased likelihood of death and is a phenomenon that occurs nearly universally throughout all the world’s organisms. This thesis initially investigated the impact of ageing on the adult Drosophila melanogaster cellular immune response and demonstrated that the cellular immune response in D. melanogaster adults did experience an age-dependent decline in function. There was a striking reduction in haemocyte ability to phagocytose foreign particles with up to 30% less phagocytosis occurring in four week old flies compared to one week olds. Haemocyte number also declined in female flies by up to 32% across these ages. An exploration into the mechanisms that could underlie these observed senescent declines in haemocyte number and function revealed that the age-dependent reduction in the circulating haemocyte population occurred regardless of whether flies were unharmed, wounded or infected. The loss of phagocytosis ability in haemocytes in ageing flies was shown to be a cell autonomous process; there was an equal age-dependent decline (~13%) in haemocyte phagocytic activity in both in vivo and ex vivo assays. However, an attempt to identify phagocytic receptor systems that drove senescence in haemocyte function was unsuccessful. The contribution of the cellular immune response in determining survival following a fungal infection was not conclusively demonstrated, however flies with reduced Dif expression had significantly increased pathogen susceptibility. Although pathogen resistance can decline due to immune senescence, disease defence may also be enhanced as an animal’s life progresses through the formation of immunological memories of prior microbial encounters. This thesis revealed that the cellular immune response in D. melanogaster provides a strong, broadly specific and relatively long-lasting immunological priming response. Haemocytes phagocytosed up to 33% more microbes per cell during a secondary encounter, and up to 50% more if flies had received two homologous primes. This was not general immune upregulation as a heterologous microbial encounter caused a reduction in the phagocytic ability of haemocytes compared to controls. The level of enhancement in the phagocytic ability of haemocytes also declined with the age of the fly, meaning that the ability to develop a primed response senesced. These results are unprecedented in Drosophila and challenge our conventional interpretation of immune senescence because individual immune history has been shown to shape later cellular immune responses. Ageing is a complex and variable process. Some of the differences observed in ageing rates between populations can be due to different selection pressures. Natural selection acts on genetic variation within a population to increase fitness whereas host-parasite interactions predominantly influence genes related to immune parameters. Many genes have pleiotropic effects as well as there being potential trade-offs between investment in longevity, reproduction and immunity. To explore potential genetic variation in immune and life history traits and whether variation in immune parameters negatively influenced other life history traits related to ageing, a panel of outcrossed genotypes of D. melanogaster were assessed. As the flies were derived from individuals originally sourced from a natural population, the results suggest that a striking amount of genetic variation in immune and life history traits is present in wild populations. However no significant correlations between genetic variation in ageing and genetic variation in investment in immunity were identified. Though, perhaps not surprisingly, no key biomarker of ageing in D. melanogaster was identified; this thesis has contributed some significant findings on the effects of ageing on adult D. melanogaster especially relating to their cellular immune response.
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Young, Lauren Jill. "Cellular immune responses of marsupials : family Macropodidae /." View thesis, 2002. http://library.uws.edu.au/adt-NUWS/public/adt-NUWS20030724.151428/index.html.

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Thesis (Ph.D.) -- University of Western Sydney, 2002.
"A thesis submitted to the University of Western Sydney in fulfilment of the requirements for the degree of Doctor of Philosophy" Bibliography : leaves 400-437.
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McAuley, Julie Louise. "MUC1 in innate and adaptive immunity /." [St. Lucia, Qld.], 2005. http://www.library.uq.edu.au/pdfserve.php?image=thesisabs/absthe19061.pdf.

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Jun, Janice. "THE OFFENSE-DEFENSE BALANCE IN IMMUNITY." Case Western Reserve University School of Graduate Studies / OhioLINK, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=case1467997330.

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26

Liew, F. Y. "Cell mediated-immunity against infectious diseases." Thesis, Canberra, ACT : The Australian National University, 1990. http://hdl.handle.net/1885/142999.

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Ahanotu, Ejemihu Ndu. "Immune Response of the Rat to Outer Membrane Proteins of Legionella pneumophila." Thesis, North Texas State University, 1985. https://digital.library.unt.edu/ark:/67531/metadc935780/.

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Outer membrane proteins (OMPs) were recovered from eleven strains (eight serogroups) of Legionella pneumophila by sequential treatment with Tris buffer (pH 8), citrate buffer(pH 2.75) and Tris buffer (pH 8). Transmission electron microscopy revealed clearly the separation of the outer membrane from the bacteria. The development of delayed hypersensitivity was also noted by measuring the area of arythema and induration produced by intradermal injections of the MPSs from Chicago 8 strain. The adjuvants enhanced greatly both active and cell-meditated immunity (CMI). Transient lymphocytopenia with a slight rise in neutrophils was noted in each of the immunized groups. Intraperitoneal challenge, seven days after the OMP booster, of one LD (1.5 x10^6) of legionellae resulted in lymphocytopenia with elevated neutrophils. All immunized rats survived the challenge, although those in the saline-OMP group were clearly the sickest. Post-challenge, legionella antibody titers rose greatly and CMI was heightened. Passive immunization (homologous and heterologous) was found to protect the rats from a challenge of on LD. Actively-immunized rats retained their immunity for at least six months as determined by their resistance to a second challenge.
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Higgins, Melanie Rae. "Identification of novel virulence factors and mechanisms of pathogenesis from the sexually transmitted protozoan Tritrichomonas foetus." Diss., Montana State University, 2006. http://etd.lib.montana.edu/etd/2006/higgins/HigginsM0506.pdf.

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29

Fatime, Ramla Tanko. "Restoration of cellular immunity in HIV-infected individuals on antiretroviral therapy." Doctoral thesis, University of Cape Town, 2017. http://hdl.handle.net/11427/25280.

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During the course of HIV pathogenesis, the virus induces multiple defects in immune cells, altering their functional ability to efficiently control HIV itself and other infections. Whilst the widespread implementation of antiretroviral therapy (ART) has led to reduced morbidity and mortality in most HIV-infected individuals having access to treatment, we still do not know whether full restoration of immune function occurs. The aim of this study was to assess the extent to which ART restores both phenotypic and functional T and B cell immunity. HIV-infected women were studied before and 1 year after ART initiation. In Chapter 2, the effect of ART on T cell activation and differentiation profiles was evaluated in HIV-infected individuals (n=28; pre- and post-ART), and compared to HIVuninfected age- and sex-matched controls (n=23). In Chapter 3, the restoration of copathogen specific CD4+ T cells was determined by comparing their cytokine secretion ability and memory differentiation profiles in response to Mycobacterium tuberculosis and cytomegalovirus in HIV-infected (n=15; pre- and post-ART), compared to uninfected (n=9) individuals. Finally, Chapter 4 examined changes in B cell activation and memory profiles in HIV-infected persons (n=19; pre- and post- ART), and compared profiles to HIV-uninfected individuals (n=19). Multiparameter flow cytometry was performed to address the study objectives. T cell activation, as measured by CD38 and HLA-DR expression, was significantly reduced one year after ART for both CD4+ and CD8+ T cells, but normalisation to levels in HIV-uninfected individuals did not occur, despite suppression of viral load. In addition, skewed CD4+ and CD8+ T cell memory profiles were not completely restored. Furthermore, no change in the cytokine production capacity and memory profile of pathogen-specific CD4+ T cells was found before and after ART, but pathogen-specific CD4+ T cells exhibiting a late differentiated profile (CD27- CD45RO+) had a lower ability to replenish (p=0.02; r = -0.5) compared to cells with an early differentiated profile (CD27+CD45RO+; p=0.04; r = 0.45) prior to ART. Similar to T cells, activated B cells (CD40+CD86+) were only partially normalised post-ART, and remained significantly higher than B cells of HIV-uninfected individuals. The frequency of all B cell memory subsets were comparable between HIV-treated and uninfected individuals, with the exception of plasmablasts, whose frequency was still significantly higher than in HIV-uninfected subjects. In summary, these results demonstrate that HIV-infected women on suppressive ART show a substantial but only partial normalisation of T cell and B cell memory subsets, and lower levels of T cell and B cell activation. In addition, restoration of co-pathogen specific memory CD4+ T cells upon treatment was dependent on their memory profile before ART. Understanding the impact of HIV on T and B cell dysfunction and restoration upon ART may provide important insights into the mechanisms of HIV pathogenesis in the era of ART.
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30

Xu, Dan. "Cellular Immunity in Recombinant Adeno-Associated Virus Vector Mediated Gene Therapy." The Ohio State University, 2011. http://rave.ohiolink.edu/etdc/view?acc_num=osu1313504203.

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31

Hollingworth, James. "The manipulation of cellular immunity by monoclonal antibodies in cancer patients." Thesis, University of Leicester, 1994. http://hdl.handle.net/2381/34109.

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The role of an immune response in the development and regulation of tumour growth is outlined. The historical development of immunotherapy in the treatment of human cancer is reviewed and the mechanisms by which immunity may be manipulated in vitro and in vivo with respect to improving cancer immunotherapy are discussed. The experimental studies and laboratory methods finally used are presented and validated in chapter 3. Non-major histocompatibility-restricted cellular cytotoxicity was assessed in a standard 4-hour 51chromium-release assay and peripheral blood cell populations were examined using fluoresceine-conjugated monoclonal antibodies and flow cytometry. Initially in vitro studies of cellular cytotoxicity against cultured tumour cells were undertaken using peripheral blood mononuclear cells (PBMC) obtained from healthy volunteers. Extremely variable levels of cellular cytotoxicity were documented in these healthy donors which were unrelated to age or sex but were positively correlated with numbers of circulating natural killer (NK) cells. The effect on cytotoxicity, of preincubating PBMC with monoclonal antibodies (mAb) and interleukin 2 (IL-2) was studied. Various mAb including those to the CD3 antigen were found to enhance cellular cytotoxicity in vitro. The mechanism of enhancement remained unproven. However, preliminary studies suggested that mAb redirected effector cells by interacting with Fc receptors on the surface of tumour cells. Combinations of mAb had a partially additive effect on enhancement of cytotoxicity. IL-2 also enhanced cytotoxicity in a dose dependent manner although synergy between IL-2 and anti-CD3 was not demonstrated. PBMC were then studied from patients with advanced gastrointestinal tract cancer. Levels of cellular cytotoxicity were not significantly related to tumour extent and were similar to cytotoxicity in healthy donors. Cytotoxicity was mediated mainly by NK cells although lymphocytes coexpressing the CD3 antigen and NK surface antigens were significantly increased in cancer patients compared with healthy donors and also in patients with liver metastases compared to those without liver involvement. In cancer patients with liver metastases, lymphocytes coexpressing the CD3 antigen and NK antigens may play a more significant role in K562 cytotoxicity. Cytotoxicity was also enhanced in vitro by anti-CD3 mAb and I1-2. A clinical study was undertaken to investigate the safety and the immunomodulating properties of administering between 50 mug and 0.5 mug of OKT3 or normal saline to patients with advanced cancer. Patients experienced minimal and self- limiting dose-related side effects. Only one patient developed evidence of cytokine release following OKT3 when assessed by enzyme-linked immunosorbent assays. Depletion of circulating T cells and NK cells occurred following OKT3 which was proportional to the dose administered. Lymphocyte activation assessed by interleukin 2 receptor expression was not detected. Considerable individual variation in cytotoxicity was related to variation in NK cell numbers in blood in both OKT3 and normal saline treated patients. 50 mug OKT3 was associated with a rapid decline in both circulating NK cells and cytotoxicity at 4 hours compared with lower doses of OKT3. The lower doses of OKT3 had a variable effect on cytotoxicity at 24 hours. 20 mug and 5 mug OKT3 was associated with a significant rise in cellular cytotoxicity at 24 hours compared with untreated controls and the 10 mug dose. These results demonstrate that anti-CD3 mAb enhance cellular cytotoxicity in vitro. The effect of OKT3 on lymphocyte function in vivo is dose-related and variable. Low doses of OKT3 may either enhance or depress cellular immunity depending upon the precise dose and time of study following administration. The relationship between the in vitro effects of anti-CD3 mAb on cellular cytotoxicity and their effects in vivo are uncertain. Although low doses of OKT3 may be safely administered to cancer patients further studies are needed to define its potential in human cancer immunotherapy.
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32

Furniss, James John. "Ubiquitin-ligase-mediated transcription initiation in cellular stress defences." Thesis, University of Edinburgh, 2016. http://hdl.handle.net/1842/22004.

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Accurate regulation of gene transcription is essential for organismal survival, and is orchestrated by myriad transcription factors and cofactors (TFs). Little is known about how the intrinsic activity of TFs is controlled. Recent work has indicated that the selective proteolysis of TFs provided by the ubiquitin-proteasome system (UPS) plays an important role in stimulating gene expression through a ‘destruction-activation’ mechanism, whereby the degradation of a ‘used’ TF is thought to stimulate further ‘fresh’ TF binding and reinitiate gene transcription. TFs are targeted to the proteasome via E3 ligases that mediate the addition of ubiquitin molecules to form a chain on the substrate TF. These polyubiquitin chains may be extended by E4 ligases, which recognize substrates with four or more ubiquitin molecules, amplifying substrate targeting to the proteasome. In plants the immune response to many pathogens is regulated by the hormone salicylic acid (SA), which operates through the transcriptional coactivator NPR1 to induce large scale changes in gene expression. Proteasome-mediated degradation of NPR1 appears to be required for the activation of its target genes. Mutation of the E3 ligase prevents ubiquitination of NPR1, leading its to stabilisation and suppression of transcription. Chapter 3 of this work identifies the first E4 ligase, UBE4, involved in NPR1 regulation. Mutation of UBE4 resulted in reduced capacity to polyubiquitinate substrates and stabilized NPR1. In contrast to E3 ligase mutants, however, mutant ube4 plants displayed increased NPR1 target gene expression. These results suggest that initial ubiquitination of NPR1 may stimulate its ability to initiate transcription and that subsequent ubiquitin chain elongation limits NPR1 activity by targeting it to the proteasome. Chapter 4 describes a ubiquitin-protein-ligase (UPL) which is both novel and crucial to the SA-mediated defence response. Mutation of this UPL leads a large reduction in total cellular polyubiquitinated proteins and was associated with strongly enhanced disease susceptibility. Gene expression profiling of upl mutants revealed an intimate connection between cellular polyubiquitination and appropriate activation of SA-responsive gene expression programmes. Destruction activation was first described in yeast and is required for the regulation of yeast amino acid synthesis TF GCN4. GCN4 requires proteasome-mediated degradation to induce genes involved in amino acid production. Chapter 5 investigates the role of two E4 ligases in GCN4 turnover. While one mutation had little effect of GCN4-mediated transcription a second increased basal transcriptional levels, suggesting that an E4 is required for the prevention of spurious GCN4-mediated transcription. In summary the work presented here describes cellular mechanisms by which global and substrate-specific polyubiqutination are vital to regulation of gene transcription.
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33

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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34

Reed, Jennifer. "Interferon-gamma increases CD4+ T cell survival and proliferation." Click here for download, 2006. http://wwwlib.umi.com/cr/villanova/fullcit?p1432655.

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35

Tran, Tinh Vi. "The hydrolysis rate of fluorescent dipeptides by dipeptidyl peptidase I (DPPI)." Thesis, Georgia Institute of Technology, 1999. http://hdl.handle.net/1853/10132.

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36

Bangham, C. R. M. "The cellular immune response to respiratory syncytial virus in mouse and man." Thesis, University College London (University of London), 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.376958.

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37

Beck, Melinda Annetta. "Regulation of cell-mediated immunity during reinfection with influenza virus /." The Ohio State University, 1987. http://rave.ohiolink.edu/etdc/view?acc_num=osu1487324944212867.

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38

Чорненька, Жанетта Анатоліївна. "CHARACTERISTIC OF INDICATORS OF CELLULAR AND HUMORAL IMMUNITY IN PATIENTS WITH DEMODECOSIS." Thesis, Материалы 72-й научно-практической конференции студентов-медиков и молодых ученых с международным участием «Актуальные проблемы современной медицины». Самарканд 11-12 мая 2018 г. С.382, 2018. http://dspace.bsmu.edu.ua:8080/xmlui/handle/123456789/14251.

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39

Lindencrona, Jan Alvar. "Enhancing T cell mediated immunity in DNA vaccination /." Stockholm, 2003. http://diss.kib.ki.se/2003/91-7349-710-x.

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40

Wilder, Sarah A. "The Relationships between Energetic Condition, Immune System Cellular Components, Testosterone Corticosterone, and Hemoparasites in Breeding Birds." Fogler Library, University of Maine, 2007. http://www.library.umaine.edu/theses/pdf/WilderSA2007.pdf.

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41

Kischnick, Christian [Verfasser], and Steeve [Akademischer Betreuer] Boulant. "Role of Phosphoinositides in Cellular Polarity and Immunity / Christian Kischnick ; Betreuer: Steeve Boulant." Heidelberg : Universitätsbibliothek Heidelberg, 2018. http://d-nb.info/1177253089/34.

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42

Schanen, Brian. "Novel Immunogens of Cellular Immunity Revealed using in vitro Human Cell-Based Approach." Doctoral diss., University of Central Florida, 2012. http://digital.library.ucf.edu/cdm/ref/collection/ETD/id/5483.

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Nanotechnology has undergone rapid expansion largely as a result of its enormous potential for applications as biomaterials, drug delivery vehicles, cancer therapeutics, and immunopotentiators. Despite this wave of interest and broad appeal for nanoparticles, evidence of their effect to the human immune system remains scarce. Concerns rise as studies on nanoparticle toxicology continue to emerge indicating that nanomaterials can be acutely toxic and can have long term inflammatory effects as seen in animal models. Based on these findings and the rise in the development of nanoparticle technologies targeting in vivo applications, the urgency to characterize nanomaterial immunogenicity is paramount. Nanoparticles harbor great potential because they possess unique physicochemical properties compared to their larger counter parts as a result of quantum-size effects and their inherent large surface area to volume ratio. These physicochemical properties govern how a nanoparticle will behave in its environment. However, researchers have only just begun to catalogue the biological effect these properties illicit. We took it upon ourselves to investigate nanoparticle size-induced effects using TiO2, one of the most widely manufactured nanoparticles, as a model. We studied these effects in dendritic cells across a human donor pool. We examined dendritic cells because they have an inimitable functional role bridging the innate and adaptive arms of immunity. From this work we found that TiO2 nanoparticles can activate human dendritic cells to become pro-inflammatory in a size-dependent manner as compared to its micron-sized counterpart, revealing novel immune cell recognition and activation by a crystalline nanomaterial. Having identified nanomaterial size as a contributing feature of nanoparticle induced immunopotentiation, we became interested if additional physicochemical properties such as surface reactivity or catalytic behavior could also be immunostimulatory. Moreover, because we witnessed a stimulatory effect to dendritic cells following nanoparticle treatment, we were curious how these nanoparticle-touched dendritic cells would impact adaptive immunity. Since TiO2 acts as an oxidant we chose an antioxidant nanoparticle, CeO2, as a counterpart to explore how divergent nanoparticle surface reactivity impacts innate and adaptive immunity. We focused on the effect these nanoparticles had on human dendritic cells and TH cells as a strategy towards defining their impact to cellular immunity. Combined, we report that TiO2 nanoparticles potentiate DC maturation inducing the secretion of IL-12p70 and IL-1?, while treatment with CeO2 nanoparticles induced IL-10, a hallmark of suppression. When delivered to T cells alone TiO2 nanoparticles induced stronger proliferation in comparison to CeO2 which stimulated TReg differentiation. When co-cultured in allogeneic T cell assays, the materials directed alternate TH polarization whereby TiO2 drives largely a TH1 dominate response, whereas CeO2 was largely TH2 bias. Combined, we report a novel immunomodulatory capacity of nanomaterials with catalytic activity. While unintentional exposure to these nanomaterials could pose a serious health risk, development and targeted use of such immunomodulatory nanoparticles could provide researchers with new tools for novel adjuvant strategies or therapeutics.
Ph.D.
Doctorate
Molecular Biology and Microbiology
Medicine
Biomedical Sciences
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43

Muindi, K. M. "Cellular lipids and immunity : characterisation of glycolipids binding the antigen presenting molecule CD1." Thesis, University of Oxford, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.670089.

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44

Hou, Lin. "The distribution and characterization of protease-activated receptors in oral mucosa and skin." Thesis, Queen Mary, University of London, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.286544.

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45

Sermersheim, Matthew Alan. "MG53 is a Novel Regulator of Inflammation and Innate Immunity." The Ohio State University, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=osu157121945938419.

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46

Liu, Zhenzhen. "The Roles of Interleukin-27 in Tumor Immunity." The Ohio State University, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=osu1354656185.

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47

Auld, Stuart Kenneth John Robert. "Fitness consequences of cellular immunity : studies with Daphnia magna and its sterilizing bacterial parasite." Thesis, University of Edinburgh, 2011. http://hdl.handle.net/1842/5779.

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Immune responses are presumed to contribute to host fitness, either by fighting off infections or via immunopathology. Research in this thesis sought to relate the magnitude of a putative immune response to infection and host and parasite fitness. The experiments and field studies presented here all focus on the interactions between the freshwater crustacean, Daphnia magna and its sterilizing bacterial endoparasite, Pasteuria ramosa, using the number of circulating haemocytes as a measure of host immune activity. I found substantial genetic variation in Daphnia’s cellular response to P. ramosa, and that Daphnia genotypes that mount the strongest cellular responses are the most likely to get infected and suffer sterilization. Thus, a strong cellular response is associated with low, as opposed to high host fitness potential. There were also some host genotypes that mounted a weaker cellular response and did not go on to suffer infection, and some that lacked a cellular response and also never suffered infection with P. ramosa. These findings led to a heuristic two-stage model for infection, where the parasite has to (1) pass from the host gut to haemolymph and then (2) successfully overcome haemolymph-based immune effectors to reproduce and achieve fitness. I also demonstrate that both the magnitude of host cellular response and likelihood of infection increases with initial parasite dose in susceptible host genotypes, and that host cellular response is associated with likely infection under both host and parasite genetic variation. Parasitised Daphnia also have substantially more circulating haemocytes than their healthy counterparts in both the laboratory and in the wild, where there is substantial genetic and environmental variation. This is one of the very few examples of how an immune response designates low host and high parasite fitness potential in a wild system. Finally, using a mixture of field study and common garden experiment, I demonstrate evolution in parasite infection traits over the course of an epidemic in a wild population, and that this evolution is associated with a decline in host abundance.
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English, Kieran. "Deciphering the cellular mechanisms promoting CD4+ T cell-dependent intrahepatic CD8+ T cell immunity." Thesis, The University of Sydney, 2022. https://hdl.handle.net/2123/27735.

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The liver is the body’s largest internal organ and assumes many important physiological and metabolic functions. It is also well-established that the liver possesses unique immunological properties and a delicate balance between tolerance and immunity exists within this large organ. CD4 T cell help to CD8 T cells has emerged as a critical factor involved in promoting robust CD8 T cell responses against viral and tumour antigens. Studies in humans and chimpanzees indicate that CD4 T cells are critical for strong intrahepatic CD8 T cell responses and the spontaneous control of hepatitis C virus and hepatitis B virus infections. However, due to limitations of current small animal models, the precise role of CD4 help in orchestrating intrahepatic CD8 T cell responses, and the mechanisms by which CD4 help is transferred to intrahepatic CD8 T cells remains poorly understood. Using an rAAV based approach to express model antigens containing both CD4 and CD8 T cell epitopes specifically in hepatocytes, we first demonstrate that CD4 help enhances the primary expansion of CD8 T cells responding to hepatocyte expressed antigens, which is critical for the generation of a large pool of memory CD8 T cells in the liver, blood and lymphoid tissues. Importantly, we decipher a novel mechanism facilitating the transfer of CD4 help to intrahepatic CD8 T cells: cognate CD40-CD40L licensing of hepatic XCR1 cDC1s in situ within portal tracts and central veins. In deciphering this mechanism, we also uncovered a previously unrecognised interconnected myeloid cell network contained within portal tracts in the steady state and following antigen expression in the liver. Together, these discoveries yield important insights into the mechanisms governing the outcome of intrahepatic immune responses, and suggest avenues for future work, with the possibility of translational research to explore novel therapies to manipulate intrahepatic immunity and hence beneficially alter outcomes in human liver diseases.
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49

Vickery, Karen. "The humoral and cellular responses to duck hepatitis B virus." Thesis, The University of Sydney, 1994. https://hdl.handle.net/2123/26913.

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Acute and chronic HBV infection and the resulting liver damage including hepatocellular carcinoma (HCC) are major health problems placing large demands on health resources. In high prevalence areas transmission occurs principally perinatally or in early childhood resulting in a high incidence of chronic life-long carriers. Progress in the study of HBV infection, replication and pathogenesis has depended to a large extent on the development of animal models such as the duck/DHBV model. Although less related to HBV than the mammalian models DHBV was used to demonstrate the unique replication strategy of hepadnaviruses and is now providing an insight into the immunological mechanisms of viral clearance or persistence. In this thesis the duck model was manipulated to provide models of both chronic carriage and acute hepatitis with viral clearance by varying the time and titre of DHBV inoculated. In addition a percutaneous needle liver biopsy which permitted multiple biopsies over a short time-span was developed. The lack of systematic studies of the avian immune response to DHBV has limited our understanding of the epidemiology, natural history and pathogenesis of DHBV infection. There is insufficient cross reaction between avian and mammalian viral antigens to permit the use of human reagents. The development of virus-specific assays has been restricted by the lack of duck-specific reagents. A radioimmunoassay to detect anti-DHBs activity in serum was established and the humoral immune response in ducks which were either experimentally inoculated or naturally exposed to DHBV infection was studied. Anti-DHBs activity was detected in a significant number of ducks from DHBV infected flocks. The anti-DHBs activity was found to pass passively from dam to offspring and neutralised DHBV infectivity in vivo. Acquired immunity may explain the variable infectivity of DHBV when injected into day-old ducklings from different flocks from similar genetic stock. Despite the importance of CMI in the pathogenesis of HBV infection the role of viral antigens in determining the outcome of infection is not clear. In order to determine the nature and timing of the specific immune response involved in clearance of infection the CMI of the duck/DHBV model was studied. Initially, the conditions were defined for optimum splenocyte responses to commonly used non-specific mitogens PHA, ConA and LPS and found to differ from those reported for peripheral blood mononuclear cells. The optimal conditions for antigen-specific mononuclear transformation were determined. The duck model was then used to study the CMI of uninfected. transiently or chronically infected and vaccinated ducks to antigenic stimulation and related these findings to humoral response and outcome of infection. The rate of clearance of viral particles from the circulation is related to the dosage given rather than the age of the duck. The infection rate of adult ducks also depends on the virus dose. In individual adult ducks with slow removal of viral inoculum or uptake of virus by blood mononuclear cells is unrelated to the development of infection. In baby ducks appearance of progeny virus occurs by 24 hours after inoculation. The lack of replication within this time frame in adult ducks or in tissue culture supernatant may reflect a higher percentage of cells refractory to infection. Adult ducks demonstrated a viraemia of limited duration and low titre while the viraemia in baby ducks was of high titre and constant. The IDso endpoint of 26-day—old ducks was found to be 1000 times the 11?0 dose of day-old ducks. A Chi-square analysis comparing livers with or without inflammation showed that DHBV positive livers had significantly (P<0.01) more inflammation than DHBV negative livers. The repeated inoculation of adult ducks with small doses of DHBV resulted in the production of neutralising antibody and anti-DI-[Bs activity. The presence of anti-DHBs activity was determined in 168 day-old duckling, 77 two month old, 20 six month old and 99 twelve month old ducks from 3 commercial farms. Significant anti-DHBs activity was detected in 1/53 ducklings from non exposed flocks compared with 28/117 ducklings hatched from DHBV infected flocks (p<0.01). Significant anti-DHBs activity was detected in only 1/40 non-exposed ducks compared with 42/ 1 56 ducks from infected flocks (p<0.01). However, naturally occurring anti-DI-[Bs levels are lower than levels obtained in the vaccinated ducks and showed a positive correlation to DHBV exposure but a negative correlation to infection. The anti-DHBS activity in day-old ducks fiom DHBV endemic flocks suggests that immunity is transferred from dam to offspring via the egg. This passively acquired anti-DHBs activity was able to neutralise DHBV infectivity in vivo in 75% of cases (p<0.02).. Optimisation of mitogen concentration for stimulation of duck splenic mononuclear cell cultures was 5x105cells/well. Once the cell concentration increased to le0 cells/well the unstimulated cultures exhibited blastogenesis and uptake of 3H thymidine, so that the high counts obtained for the mitogen stimulated cultures were not significantly different from those obtained for unstimulated controls. Cell numbers below 5x105cells/well resulted in decreased 3I-I thymidine uptake and lower SI. The response to each mitogen was different and there was also substantial duck to duck variation in response to mitogen stimulation. PHA at concentrations between 5 and 20pg/ml, produced good transformation (SI>3 00) from day l to 4 of culture. Peak transformation was achieved with Con A concentrations of between 10 to 20ug/ml for all four ducks tested. The transformation of SMC in response to LPS was poor when compared with that obtained with PHA or Con A in the three ducks tested. The concentration of LPS required to give maximal transformation responses varied between 10 and 40ug/ml and resulted in SI of up to 20.The optimum cell concentration for peripheral blood mononuclear cells (PBMC) varied between ducks and in order to maximise antigen or mitogen, cell concentrations needed to be optimised on an individual basis. Maximum antigen-specific transformation varied from duck to duck but occurred between days 4 and 7. The optimum antigen concentration varied between ducks from 1 to lOOOng/ml for DHBsAg and between 10 and lOOng/ml for DHBcAg. As expected the level of transformation (SI) was not as great as that obtained with stimulation with PHA which would be expected to stimulate a greater number of cells non-specifically. However, the antigen specific transformation response was similar to that obtained by stimulation with LPS. In acute DHBV infection PBMC from 2/8 and 3/8 responded to stimulation core or surface antigen respectively with one duck responding to both antigens. Both ducks that responded to core antigen cleared DHBV from the serum and the liver, while the ducks that responded to surface antigen cleared DHBV DNA from the serum , albeit only temporary in R89.In ducks that developed chronic DHBV infection 3/5 and 2/5 ducks responded to core and surface antigen respectively. The two ducks with the greatest liver pathology responding to DHBsAg. Vaccination with the 17kDa S protein produced a poor immunological response in the majority of ducks with only 2/4 responding with significant DHBsAg specific proliferation and one with concurrent anti-DHBs production. In the majority of immune ducks whether vaccinated or convalescent from infection the PBMC responded to stimulation by both antigens following a challenge with DHBV. However, this CMI response was temporary falling to non-significant levels quickly. The two sample Wilcoxon's rank sum test was applied to test for any significant difference between the above groups. The PBMC transformation response to both surface and core antigen in the immune ducks following challenge was significantly different from the transformation responses obtained from non-exposed ducks and ducks acutely infected with DHBV (P<0.05).
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50

De, la Rosa Patricia. "Changes in immune cell populations and the antibody response to Streptococcus pneumoniae after exposure to a mixture of herbicides." Morgantown, W. Va. : [West Virginia University Libraries], 2003. http://etd.wvu.edu/templates/showETD.cfm?recnum=2929.

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Thesis (Ph. D.)--West Virginia University, 2003.
Title from document title page. Document formatted into pages; contains xii, 243 p. : ill. Vita. Includes abstract. Includes bibliographical references (p. 213-240).
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