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Dissertations / Theses on the topic 'Lymphocyte'
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1
Culley, Donald A. "Recognition of carbohydrates by T lymphocytes in lymphocyte activation." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape11/PQDD_0022/NQ50137.pdf.
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Culley, Donald A. "Recognition of carbohyrates by T lymphocytes in lymphocyte activation." Thesis, McGill University, 1997. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=35686.
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The purpose of this investigation was to elucidate the role of the oligosaccharides of Class II MHC glycoproteins in allostimulation. Plasma membranes (PM) from the Daudi cell line were chemically deglycosylated using anhydrous hydrogen fluoride (HF). Subsequently, native and deglycosylated (dgl) Class II MHC molecules were affinity purified from their respective PM and inserted into the PM of peripheral blood leukocytes (PBL) which were used as stimulators in the mixed leukocyte reaction (MLR). Stimulator and responder cells were from the same donor. Both forms of the antigen were found to elicit a proliferative and cytolytic (CML) response but the dgl antigen did so to a lesser extent. Thus, it seemed as though the oligosaccharide side chains of Class II MHC molecules may not be required for allostimulation. A similar reduction in the cytolytic response was obtained when effector cells generated by the native antigen were used against targets that were stripped of N-linked oligosaccharides by tunicamycin (TM) pretreatment. Twenty-four clones were raised against the native antigen. Three clones gave proliferative responses only to the native antigen while two clones responded equally to both native and dgl antigen. In CML studies the three clones lysed normal targets but failed to lyse TM-treated target cells while the two clones did not discriminate between the two targets. Accordingly, the three clones were termed anti-MHC oligosaccharide clones while the two clones were termed anti-MHC polypeptide clones. In inhibition of CML experiments using the dgl supernatant which contained Daudi PM oligosaccharide or using a anti-MHC class II monoclonal antibody; CML reactivity of the anti-MHC oligosaccharide clones was blocked by the dgl supernatant but not by the anti-MHC MoAb. On the other hand the anti-MHC polypeptide clones were only inhibited by the anti-MHC MoAb whether against intact or TM-treated targets. These studies strongly indicate that glycoconjugates of
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Bonnefoy-Berard, Nathalie. "Induction et régulation de l'activation des lymphocytes T et B par les globulines antilymphocytaires." Lyon 1, 1992. http://www.theses.fr/1992LYO1H086.
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Greenwood, M. R. "B lymphocyte differentiation." Thesis, Imperial College London, 1986. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.375109.
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Jefferies, W. A. "Lymphocyte surface glycoproteins." Thesis, University of Oxford, 1985. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.355757.
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McCrea, Anthony Philip. "The role of the T lymphocyte in B cell chronic lymphocytic leukaemia." Thesis, Queen's University Belfast, 1989. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.335939.
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Moris, Arnaud. "On T lymphocyte alloreactivity." [S.l. : s.n.], 2000. http://www.bsz-bw.de/cgi-bin/xvms.cgi?SWB8849701.
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Bonnefoix, Thierry. "Les lymphocytes T intra-tumoraux dans les lymphomes malins non hodgkiniens B : activation, prolifération et production de facteurs de régulation des cellules B." Grenoble 1, 1991. http://www.theses.fr/1991GRE10153.
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Les lymphocytes t sont constamment presents dans les ganglions envahis par un lymphome malin non hodgkinien b. Ce travail a permis de reunir des arguments en faveur de l'implication de ces cellules t dans le processus tumoral: diminution de la capacite des cellules t a produire de l'interleukine 2 (il2) et a proliferer en presence de pha; pourcentages eleves de cellules t dr+ (activees), et cd4+cd45ra-(memoires), ainsi que de cellules t cd25+ (p55 du recepteur de l'il2); a partir des cellules t cd25+ totales, il a ete obtenu des clones t capables de proliferer au contact des cellules b malignes autologues, mais pas au contact des cellules b normales (b-ebv) autologues; la nature des relations fonctionnelles entre les cellules t intra-tumorales et les cellules b malignes autologues reste a determiner: en utilisant des cellules b normales comme cibles des cellules t, il n'a pu etre mis en evidence aucune anomalie de production d'activites bcgf et bcdf mu et gamma
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Lumbroso, Serge. "Production spontanée in vitro par les lymphocytes circulants d'anticorps spécifiques de Brucella." Montpellier 1, 1990. http://www.theses.fr/1990MON11228.
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Barré, Vincent. "La leucemie a grands lymphocytes granuleux : a propos d'un cas ; revue de la litterature." Nice, 1992. http://www.theses.fr/1992NICE6541.
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Rigal, Dominique. "Action de l'histamine sur la physiologie des lymphocytes : synthèse bibliographique et apport personnel." Lyon 1, 1987. http://www.theses.fr/1987LYO1H073.
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Cox, A. L. "Lymphocyte homeostasis and autoimmunity following therapeutic lymphocyte depletion in the treatment of multiple sclerosis." Thesis, University of Cambridge, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.598102.
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Campath-1H induces immediate lymphocyte depletion and remission of inflammatory disease activity when used to treat multiple sclerosis. A cohort of 16 people with multiple sclerosis were studied for one year following a single pulse of Campath-1H treatment. In addition to reporting on their clinical course, serial detailed immunological investigations were performed focusing on immunoregulation and homeostasis. Two phases of lymphocyte reconstitution following Campath-1H treatment were observed. In the first six months lymphocyte proliferation increased and the residual T cell pool was dominated by memory T cells, especially regulatory T cells. In the later phase these changes reversed. The relative fall in regulatory T cell numbers coincided with a period of susceptibility to novel autoimmunity offering a mechanism by which proliferating auto-reactive T cells might escape control. Total CD4+ numbers remained below 50% of pre-treatment levels at twelve months despite a sustained increase in IL-7. However CCL21 and Il-15 responses to lymphopaenia appear to be suboptimal explaining the delayed lymphocyte reconstitution. Auto-reactive lymphocytes exist in the normal T Cell repertoire. As exposure to myelin antigens may result in autoimmune type activation of T cells, lymphocyte responses were investigated in 10 head injury patients. Proliferation and cytokine production following <i>ex vivo</i> exposure to myeline protein was generally suppressed. However, some individuals demonstrated increased reactivity and reduced TGF-b expression suggesting relatively less regulation of auto-reactivity.
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Weiss, David M. "Cancer-Specific Stress and Absolute Lymphocyte Count Trajectories in Patients with Chronic Lymphocytic Leukemia." The Ohio State University, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=osu147765209495775.
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Du, Zhenjian Cheung H. Tak. "Febrile condition and lymphocyte proliferation." Normal, Ill. Illinois State University, 1991. http://wwwlib.umi.com/cr/ilstu/fullcit?p9203029.
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Thesis (Ph. D.)--Illinois State University, 1991.<br>Title from title page screen, viewed December 8, 2005. Dissertation Committee: H. Tak Cheung (chair), Herman E. Brockman, Lynne A. Lucher, Anthony J. Otsuka, Alan J. Katz. Includes bibliographical references (leaves 99-110) and abstract. Also available in print.
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Mallett, Susan. "Characterization of T lymphocyte antigens." Thesis, University of Oxford, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.293461.
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Carolan, E. J. "Gap junctions in lymphocyte ontogeny." Thesis, University of Glasgow, 1985. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.233181.
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Bleakey, Jill Susanna. "Evaluating canine T lymphocyte responses." Thesis, University of Liverpool, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.364348.
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Edwards, M. R. "Lymphocyte dysfunction and postoperative morbidity." Thesis, University College London (University of London), 2014. http://discovery.ucl.ac.uk/1420997/.
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Morbidity following major surgery is a growing healthcare problem. Previous studies have shown associations between preoperative lymphopenia and adverse postoperative outcomes, albeit in patient groups with multiple confounding factors. Lymphopenia is also associated with poor outcomes in a range of chronic and acute disease states including cardiac failure and sepsis, where lymphocyte dysfunction and excess lymphocyte apoptosis is observed. Cellular bioenergetic failure has been observed in these disease states and is proposed as a key pathophysiological mediator. The core hypothesis of this thesis is that preoperative lymphopenia is associated with increased morbidity after a standardized physiological insult due to underlying bioenergetic dysfunction. A large observational cohort study in patients undergoing elective lower limb arthroplasty showed preoperative lymphopenia to be a common phenomenon independently associated with increased postoperative morbidity and length of hospital stay. Further analysis of a subset of this cohort showed lymphopenia to be a chronic feature, not associated with common diagnoses known to cause lymphopenia. Immunophenotyping using flow cytometry confirmed lymphopenia affecting all lymphocyte subsets, but with normal monocyte and neutrophil number and function. Lymphocyte function was further explored using ex-vivo culture experiments in normal and lymphopenic subjects. In lymphopenic patients, lymphocyte apoptosis in response to a variety of insults was increased and ex-vivo stimulated lymphocyte proliferation was reduced. A novel experimental model was developed to assess lymphocyte bioenergetic function, using respirometry to assess glycolysis and mitochondrial function in freshly isolated cells. Lymphocytes from lymphopenic patients had global reductions in bioenergetic function and intracellular ATP content. In summary, chronic lymphopenia is common in the elective orthopaedic population and is robustly associated with adverse postoperative outcomes. The data here characterise a patient phenotype at increased perioperative risk. The underlying cellular dysfunction described may have important implications in a range of acute and chronic illnesses.
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Pereira, Cátia Daniela Isaías. "Lymphocyte populations in Mucopolysaccharidosis patients." Master's thesis, Universidade de Aveiro, 2015. http://hdl.handle.net/10773/15580.
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Mestrado em Biomedicina molecular<br>As doenças de sobrecarga lisossomal (DSLs) constituem um grupo de distúrbios metabólicos raros maioritariamente causados por mutações em hidrolases lisossomais, que conduzem à acumulação anormal de diferentes substratos macromoleculares no interior do lisossoma. Este trabalho é focado nas mucopolissacaridoses (MPSs), um grupo de DSLs resultantes da atividade deficiente de enzimas envolvidas no catabolismo dos glicosaminoglicanos. A MPS II é caraterizada pela perda de atividade da enzima iduronato-2-sulfatase, levando ao armazenamento intralisossomal de sulfato de dermatano e sulfato de heparano. A MPS VI é definida pela acumulação de sulfato de dermatano dentro do lisossoma, devido a uma deficiência na atividade enzimática de arilsulfatase B. O lisossoma é um compartimento celular importante para o funcionamento normal do sistema imunitário. Em diversos modelos de DSLs, foram anteriormente descritas alterações nas células do sistema imunitário. Os principais objetivos do presente trabalho eram: (i) estudar as várias populações leucocitárias – incluindo células T e seus subconjuntos, células natural killer (NK), células B e suas subpopulações, e monócitos – no sangue periférico de doentes com MPS II e MPS VI; (ii) produzir linhas de células B transformadas pelo vírus Epstein–Barr (EBV) destes pacientes, assim como avaliar a eficácia na sua produção e determinar o seu fenótipo. A caraterização do sistema imunitário nas doenças MPS II e MPS VI revelou um decréscimo significativo na frequência de células NK e monócitos em doentes com MPS VI, mas não em doentes com MPS II, em comparação com indivíduos controle. Em contraste, não foram identificadas alterações na percentagem de células T, células natural killer T invariantes (iNKT) e células B nos grupos de doentes com MPS II e MPS VI, comparando com o grupo controlo. A análise detalhada do estado de memória de células T auxiliares e células T citotóxicas revelou desequilíbrios nos fenótipos naïve e de memória em ambos os compartimentos de células T em doentes com MPS VI, mas não em doentes com MPS II, em comparação com indivíduos controle. As linhas de células B transformadas pelo EBV foram produzidas com sucesso nos dois grupos de doentes com MPS, mas a eficácia na sua produção foi superior no caso dos doentes com MPS VI, comparando com os indivíduos controle e doentes com MPS II. O fenótipo predominante das linhas de células B transformadas pelo EBV era similar entre ambos os grupos de doentes com MPS e o grupo controlo, o qual foi avaliado como sendo correspondente à subpopulação de células B de memória duplamente negativas. Em conclusão, este trabalho permitiu caraterizar melhor o sistema imunitário nestas duas doenças raras.<br>Lysosomal storage diseases (LSDs) constitute a group of rare metabolic disorders mostly caused by mutations in lysosomal hydrolases, which conduce to abnormal accumulation of different macromolecular substrates inside the lysosome. This work is focused on the mucopolysaccharidoses (MPSs), a group of LSDs arising from the deficient activity of enzymes involved in the catabolism of glycosaminoglycans. The MPS II is characterized by loss of activity of the enzyme iduronate-2-sulfatase, leading to the intralysosomal storage of dermatan sulfate and heparan sulfate. The MPS VI is defined by the accumulation of dermatan sulfate within the lysosome, owing to a deficiency in the enzymatic activity of arylsulfatase B. The lysosome is an important cellular compartment for the normal functioning of the immune system. In several models of LSDs, alterations in the immune system cells were previously described. The main aims of the present work were: (i) to study the various leukocyte populations – including T cells and their subsets, natural killer (NK) cells, B cells and their subpopulations, and monocytes – in the peripheral blood of MPS II and MPS VI patients; (ii) to produce Epstein–Barr virus (EBV)- -transformed B cell lines from these patients, as well as to evaluate the efficacy in their generation and determine their phenotype. The characterization of the immune system in MPS II and MPS VI diseases revealed a significant decrease in the frequency of NK cells and monocytes in MPS VI patients, but not in MPS II patients, in comparison with control subjects. In contrast, no alterations were identified in the percentage of T cells, invariant natural killer T (iNKT) cells, and B cells in the groups of MPS II and MPS VI patients comparing with the control group. The detailed analysis of the memory state of helper T cells and cytotoxic T cells revealed imbalances in the naïve and memory phenotypes in both T cell compartments in MPS VI patients, but not in MPS II patients, as compared with control subjects. The EBV-transformed B cell lines were successfully produced in the two MPS patient groups, but the efficacy in their generation was higher in the case of MPS VI patients when comparing with control subjects and MPS II patients. The predominant phenotype of EBV-transformed B cell lines was similar between both groups of MPS patients and the control group, which was assessed as corresponding to the double-negative memory B cell subpopulation. In conclusion, this work allowed to better characterize the immune system in these two rare diseases.
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Aucher, Anne. "Étude des caractéristiques de la capture de fragments de membrane par trogocytose par les lymphocytes T et B." Toulouse 3, 2008. http://thesesups.ups-tlse.fr/752/.
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La mise en place des réponses immunitaires a lieu via l'échange de facteurs solubles et la transmission de signaux intracellulaires. Ces dernières années, un nouveau mode de communication a été découvert, mettant en jeu l'échange de fragments de membrane entre cellules en contact. Ce processus, nommé trogocytose, initialement décrit chez les lymphocytes T, est rapide, efficace et présente une spécificité de passage. Mais ses mécanismes et ses rôles physiologiques sont encore mal définis. Mon travail de thèse s'est orienté sur deux axes : mener une étude comparative des mécanismes de la trogocytose entre les lymphocytes T et B et identifier les bases de la sélectivité de capture par trogocytose. En utilisant des inhibiteurs de différentes voies d'activation lymphocytaire, nous avons déterminé que si la trogocytose est un phénomène actif, dépendant du cytosquelette d'actine et de la signalisation dans les lymphocytes T, c'est un phénomène passif dans les lymphocytes B, qui a lieu dans toutes les conditions testées. Cette différence, intrinsèque au type cellulaire, est une première étape vers la compréhension du phénomène dans son ensemble. Dans les travaux sur la sélectivité de passage par trogocytose nous avons tout d'abord montré que les glycoconjugués membranaires étaient capturés efficacement par les lymphocytes par trogocytose. L'étude a alors été complétée par une approche plus fine de criblage de protéines individuelles. Nos résultats préliminaires confirment l'existence d'une sélectivité de passage et identifient des protéines candidates, dont l'étude permettra de comprendre les bases du transfert sélectif et donc de mieux appréhender les mécanismes de la trogocytose<br>Establishment of immune responses takes place through soluble factors exchange and intracellular signals transmission. Recently, a new mode of communication has been discovered, involving the exchange of plasma membrane fragments between cells in contact. This phenomenon, called trogocytosis, originally described in T cells, occurs rapidly and efficiently and is a selective process. However, its mechanisms and physiological roles are not well defined yet. My thesis work has focused on two main areas: first to compare the mechanisms of trogocytosis in T and B lymphocytes and second to identify the criteria that determine the selectivity of transfer. Using a large panel of inhibitors of various cellular activities, we determined that trogocytosis is an active phenomenon in T cells, dependent on actin cytoskeleton and signalisation, and that it is a passive phenomenon in B cells, that can takes place in all conditions we tested. This difference, intrinsic to the cell type, is a first step towards understanding the phenomenon of trogocytosis as a whole. Concerning selectivity of molecules transfer, we first showed that glycoconjugates were captured from the target cells with the same efficiency as proteins or lipids during trogocytosis by T and B cells. In a second study, we are currently working to define the criteria of transfer selectivity of membrane components by following the transfer of unique proteins. Our initial results confirm that there is a selectivity of transfer and identify candidate proteins, whose study will enable us to understand the factors determining the transfer of molecules, and thus to advance our understanding of the mechanism(s) of trogocytosis
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Liu, Anquan. "Proinflammatory factor mediated lymphocyte activation - the pivotal role of leukotriene B4 /." Stockholm, 2007. http://diss.kib.ki.se/2007/978-91-7357-391-7/.
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Lemoine, Sébastien. "Étude du rôle du lymphocyte B dans la tolérance périphérique." Brest, 2011. http://www.theses.fr/2011BRES2308.
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Le système immunitaire est équipé de nombreux points de contrôle pour maintenir la tolérance et prévenir l'autoimmunité. Les mécanismes opérant en périphérie sont principalement médiés par les lymphocytes T régulateurs. Dans le contexte de l’autoimmunité, les lymphocytes B sont généralement considérés pathogéniques car produisant des anticorps pouvant causer des dommages aux tissus ciblés. Cependant leur déplétion dans plusieurs modèles murins de maladies autoimmunes induit une pathologie plus sévère, donnant ainsi aux lymphocytes B un rôle régulateur insoupçonné. Des pistes ont été découvertes chez la souris quant au mécanisme d’action et au phénotype de ces cellules B régulatrices et deux sous populations de lymphocytes B sécrétant de l'interleukine 10 ont été décrites. Cependant malgré un intérêt croissant pour la biologie des lymphocytes B régulateurs, l’existence d’une population équivalente chez l’homme est toujours controversée. Cette étude montre que les lymphocytes T activés peuvent induire leur propre régulation par un mécanisme qui dépend des lymphocytes B. Les lymphocytes B régulateurs identifiés comme CD19high IgD+ CD24high CD38high CD5high, inhibent la prolifération et la sécrétion des cytokines pro-inflammatoires des lymphocytes TH1. Deux mécanismes distincts sont requis. L’inhibition des sécrétions des lymphocytes T fait intervenir l’interleukine 10 sécrétée par les lymphocytes B et l’inhibition de la prolifération des lymphocytes T fait appel à l’induction de lymphocytes T régulateurs. L’évaluation de cette nouvelle fonction régulatrice dans les maladies autoimmunes montre que la régulation médiée par les lymphocytes B est déficiente dans le Lupus Erythémateux Disséminé<br>Nature has provided the immune system with numerous checkpoints controlling the maintenance of tolerance and the prevention of autoimmunity. The regulatory mechanisms operating in the periphery of the immune system are mediated mainly by a specific population of regulatory T cells considered as the main contributor to peripheral tolerance. In auto immunity, B cells are generally considered pathogenic since they release autoantibodies, that can cause damages to target tissues. However B cell depletion in several murine models of autoimmune diseases leads to a more severe pathology, giving B cells an unexpected regulatory role. Insights have been realized concerning the mechanism of action and the phenotype of this particular subset of regulatory B cells in mice and two subsets of IL-10 secreting B cells have been endowed with regulatory properties. However, despite increasing interest in regulatory B cell biology, the existence of an equivalent population in human is still a matter of controversy. The current study indicates that activated T cells can induce their own regulation by promoting the development of a B-cell dependent regulatory process. Regulatory B cells, identified by their expression of CD19high IgD+ CD24high CD38high CD5high, inhibit the proliferation and cytokine secretion of proinflammatory TH1 cells with the contribution of regulatory T cells, placing B cells at the center of immunosuppressive reactions. The assessment of this new regulatory function in autoimmune diseases shows that B-cell mediated immune regulation is deficient in Systemic Lupus Erythematosus
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Denépoux, Stéphane. "Induction de mutations somatiques des gènes d'immunoglobuline dans les lymphocytes B humain in vitro." Lyon 1, 1998. http://www.theses.fr/1998LYO1T045.
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Putheti, Prabhakar. "CD4+CD25+ T regulatory cells in multiple sclerosis /." Stockholm, 2004. http://diss.kib.ki.se/2004/91-7349-962-5.
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Karlsson, Håkan. "Influence of FK506 on certain aspects of lymphocyte activation and lymphocyte-endothelial cell interactions in vitro." Lund : Dept. of Medical Microbiology, Section of Clinical Immunology, Lund University, 1997. http://catalog.hathitrust.org/api/volumes/oclc/39799195.html.
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Han, Shuhua. "β-lymphocyte differentiation in the periphery." Thesis, Imperial College London, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.326157.
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Morrow, Michelle Ann. "Identification of genes controlling lymphocyte development." Thesis, University of Cambridge, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.620377.
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Watson, Martin Peter. "Lymphocyte costimulation in corneal allograft rejection." Thesis, Imperial College London, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.498610.
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McNeil, Christopher John. "Glutamine and lymphocyte metabolism of sheep." Thesis, University of Newcastle Upon Tyne, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.391973.
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Van, Wely Catherine Ann. "Cytokines, lymphocyte surface molecules and homing." Thesis, University College London (University of London), 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.298867.
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Matthews, Philip Trystan. "Viral interference with T lymphocyte recognition." Thesis, University of Cambridge, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.621627.
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Paterson, Alastair Glen. "Lymphocyte function in human breast cancer." Thesis, University of Edinburgh, 1988. http://hdl.handle.net/1842/20091.
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Griffin, Sara L. "Macrophages and lymphocyte responsiveness to mitogen." Thesis, Aston University, 1998. http://publications.aston.ac.uk/12351/.
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Purified B-cells fail to proliferate in response to the strong thymus-independent (TI) antigen Lipopolysaccharide (LPS) in the absence of macrophages (Corbel and Melchers, 1983). The fact that macrophages, or factors derived from them are required is supported by the inability of marginal zone B-cells in infants to respond to highly virulent strains of bacteria such as Neisseria meningitidis and Streptococcus pneumoniae (Timens, 1989). This may be due to the lack of CD21 expression on B-cells in infants which could associate with its co-receptor (C3d) on adjacent macrophages. It is not clear whether cell surface contacts and/or soluble products are involved in lymphocyte-macrophage interactions in response to certain antigens. This thesis describes the importance of the macrophage in lymphocyte responses to T-dependent (TD) and TI antigens. The major findings of this thesis were as follows: (1). Macrophages were essential for a full proliferative response to a range of T - and B-cell mitogens and TI-1 and TI-2 antigens, including Concanavalin A, LPS, Pokeweed mitogen (PWM), Dextran sulphate, Phytohaemagglutinin-P (PHA-P) and Poly[I][C]. (2). A ratio of 1 macrophage to 1000 lymphocytes was sufficient for the mitogens to exert their effects. (3). The optimal conditions were established for the activation of an oxidative burst in cells of the monocyte/macrophage lineage as measured by luminometry. The order of ability was OpZ >PMA/lonomycin >f-MLP >Con A >DS >PHA >Poly[I][C] >LPS >PWM. Responses were only substantial and protracted with OpZ and PMA. Peritoneal macrophages were the most responsive cells, whereas splenic and alveolar macrophages were significantly less active and no response could be elicited with Kupffer cells, thus demonstrating heterogeneity between macrophages. (4). Activated macrophages that were then fixed with paraformaldehyde were unable to restore mitogenic responsiveness, even with a ratio of 1 macrophage to 5 lymphocytes. (5). Although highly purified T- and B-cells could respond to mitogen provided live macrophages were present, maximum activation was only observed when all 3 cell types were present. (6). Supernatants from purified macrophage cultures treated with a range of activators were able to partially restore lymphocyte responses to mitogen in macrophage-depleted splenocyte cultures, and purified T - and B-cell cultures. In fact supernatants from macrophages treated with LPS for only 30 minutes could restore responsiveness. Supernatants from OpZ treated macrophages were without effect. (7). Macrophage supernatants could not induce proliferation in the absence of mitogen. They therefore provide a co-mitogenic signal required by lymphocytes in order to respond to mitogen. (8). Macrophage product profiles revealed that LPS and Con A-treated macrophage supernatants showed elevated levels of IL-1β, TNF -α L TB4 and TXB2. These products were therefore good candidates as the co-mitogenic factor. The possible inhibitory factors secreted by OpZ-treated macrophages were PGE2, IL-10 and NO. (9). The removal of cytokines, eicosanoids and TNF-α from LPS-treated macrophage supernatants using Cycloheximide, Dexamethasone and an MMPI respectively, resulted in the inability of these supernatants to restore macrophage-depleted lymphocyte responses to mitogen. (10). rIL-1β and rTNF-α are co-mitogenic factors, as macrophage-depleted lymphocytes incubated with rIL-1β and rTNF-α can respond to mitogen.
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Tamang, David L. "Modulation of T lymphocyte cytotoxic potential." abstract and full text PDF (free order & download UNR users only), 2008. 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:3307587.
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Van, Reyk David Marc. "Oxidative phenomena in T lymphocyte activation." Thesis, The University of Sydney, 1997. https://hdl.handle.net/2123/27622.
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Murine lymph node cells (LNC) were used as model for the assessment of a role
for reactive oxygen species (ROS) in T lymphocyte activation. When 2’7’- dichlorofluorescin (DCFHz) is oxidised it becomes the fluorescent compound dichlorofluorescein. Analysis of DCFHz-loaded LNC by flow cytometry identified an increase in DCFH2 oxidation upon stimulation with a mitogenic dose of the phorbol ester,
phorbol myristate acetate. This could also be seen, although to a lesser extent, with a mitogenic dose of the lectin concanavalin A. The phorbol ester-induced increase in DCFH2 oxidation was inhibited by chelerythrine and desferrioxamine (the latter at concentrations lower than that required for maximal inhibition of lymphoproliferation in vitro), indicating a role in DCFHZ oxidation for protein kinase C and iron, respectively. Analysis of LNC prelabelled with an antibody against a pan-T lymphocyte marker, Thy-1, established that phorbol ester treatment of LNC induces an increase in DCFHZ oxidation in murine T lymphocytes.
The inhibition of DCFH2 oxidation in LNC by superoxide dismutase, catalase and glutathione/glutathione peroxidase suggested that the source of oxidants may have been B lymphocytes and/or phagocytic cells within the population and that the oxidation in T lymphocytes essentially represented a "bystander effect". This was supported by
preliminary studies where there was little or no response to phorbol ester stimulation in DCFHz-loaded LNC from mice lacking a functional NADPH oxidase (gp91Ph0X gene knockout mice).
Studies of cell-free oxidation of DCFH2 demonstrated that the fluorogen could be oxidised by peroxyl radicals from either chemical (2,2'-azobis(2-amidinopropane) dihydrochloride) or enzymatic (soybean lipoxygenase) sources.
Finally, the role of iron in T lymphocyte activation was investigated using the iron chelators desferrioxamine and a set of novel pyridoxal-based compounds. The novel iron chelators were of comparable or greater potency compared to desferrioxamine with regard to inhibition of lymphoproliferation in vitro. Time course studies confirmed previous
reports by showing that a major target of iron chelators in activated T lymphocytes are events late in G1 or at the G1/S transition of the cell cycle.
These studies: highlight the technical difficulties of assaying oxidant production using mixed populations of cells; support the notion that DCFH2 is a general target for radical-mediated oxidation; and confirm a critical role for iron in DNA synthesis in activated T lymphocytes.
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Obino, Dorian. "Molecular mechanisms regulating B lymphocyte polarization." Thesis, Sorbonne Paris Cité, 2016. http://www.theses.fr/2016USPCB031/document.
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Dans les organes lymphoïdes secondaires, les lymphocytes B acquièrent des antigènes immobilisés à la surface de cellules voisines. L’engagement du BCR (récepteur des cellules B) avec de tels antigènes induit la formation d’une synapse immunologique et la polarisation des lymphocytes B. Cette polarisation inclut le repositionnement du centrosome à la synapse immunologique ainsi que le recrutement et la sécrétion locale des lysosomes qui sont nécessaires à l’extraction, l’apprêtement et la présentation des antigènes sur les molécules du complexe majeur d’histocomptabilité de classe II (CMH-II) aux lymphocytes T CD4+ pré-activés. Des travaux précurseurs menés dans le laboratoire ont permis de mettre en évidence les premiers acteurs moléculaires impliqués dans ce processus. Cependant, le mécanisme précis gouvernant la polarisation du centrosome demeure encore aujourd’hui inconnu. Le travail réalisé pendant cette thèse avait pour objectif d’identifier de nouveaux régulateurs contrôlant la polarisation du centrosome dans les lymphocytes B après engagement du BCR avec des antigènes immobilisés. De plus, au regard du rôle grandissant joué par le microenvironnement tissulaire dans l’activation des lymphocytes B ainsi que dans la modulation de leurs fonctions, nous avons étudié l’effet de la protéine extracellulaire Galectine-8 sur la régulation de la capacité des lymphocytes B à se polariser et à extraire et présenter des antigènes immobilisés. Le travail présenté dans ce manuscrit montre que la présence du complexe Arp2/3 au centrosome des lymphocytes B non activés permet la nucléation locale de filaments d’actine qui permettent, grâce à leur interaction avec le complexe LINC, de lier le centrosome au noyau. L’activation des lymphocytes B induit la déplétion partielle du complexe Arp2/3 du centrosome qui est recruté à la synapse immunologique par la protéine HS1. Ceci induit une diminution de la nucléation d’actine au centrosome entraînant la séparation entre le centrosome et le noyau et permettant la polarisation du centrosome vers la synapse. De plus, nous montrons que la présence de la protéine Galectine-8 dans le milieu extracellulaire favorise le recrutement et la sécrétion des lysosomes à la synapse immunologique, conférant aux lymphocytes B une meilleure capacité à extraire et présenter des antigènes immobilisés. Nos résultats mettent en évidence des mécanismes inattendus régulant la polarisation des lymphocytes B en réponse à une stimulation antigénique et soulèvent des questions intéressantes concernant la régulation coordonnée de ces mécanismes qui confèrent aux lymphocytes B la capacité d’extraire, d’apprêter et de présenter des antigènes immobilisés efficacement<br>In secondary lymphoid organs, B cells acquire antigens that are tethered at the surface of neighboring cells. Engagement of the B cell receptor (BCR) with such immobilized antigens leads to the formation of an immune synapse and the subsequent polarization of B cells. This includes the repositioning of the centrosome towards the immune synapse as well as the recruitment and local secretion of lysosomes required for efficient antigen extraction, processing and presentation onto class II major histocompatibility complex (MHC-II) molecules to primed CD4+ T cells. Pioneer work performed in the lab has highlighted the first molecular players involved in this process. However, the precise mechanism governing centrosome polarization remains to be fully elucidated. The work performed during this thesis aimed at identifying new regulators supporting centrosome polarization in B lymphocytes upon BCR engagement with immobilized antigens. In addition, in view of the emerging role played by the tissue microenvironment in shaping B cell activation and functions we investigated whether extracellular Galectin-8 modulates the ability of B cells to polarize, extract and present immobilized antigens. We show here that, in resting lymphocytes, centrosome-associated Arp2/3 (actin related protein-2/3) locally nucleates F-actin, which is needed for centrosome tethering to the nucleus via the LINC (linker of nucleoskeleton and cytoskeleton) complex. Upon lymphocyte activation, Arp2/3 is partially depleted from the centrosome as a result of its HS1-dependent recruitment to the immune synapse. This leads to a reduction in F-actin nucleation at the centrosome and thereby allows its detachment from the nucleus and polarization to the synapse. In addition, we show that extracellular Galectin-8 favors lysosome recruitment and secretion at the immune synapse, hence providing B cells with an enhanced capacity to extract and present immobilized antigens. Our findings highlight unexpected mechanisms that tune B cell polarity in response to antigenic stimulation and raise exciting questions concerning the coordinated regulation of these mechanisms to provide B cells with the capacity to efficiently extract, process and present surface-tethered antigens
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Llory, Jean-François. "Etude structurale et dynamique de la membrane du lymphocyte B dans la leucémie lymphoi͏̈de chronique." Montpellier 1, 1989. http://www.theses.fr/1989MON11288.
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Amel, Kashipaz Mohammad Rasoul. "Investigations of cytokine production by lymphocytes and autologous mixed lymphocyte reaction in relation to systemic lupus erythematosus." Thesis, Nottingham Trent University, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.272764.
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Gargett, Caroline Eve, and mikewood@deakin edu au. "Studies of the human lymphocyte P2Z receptor and its activation of phospholipase D." Deakin University, 1997. http://tux.lib.deakin.edu.au./adt-VDU/public/adt-VDU20060727.144101.
Full textAbstract:
Extracellular adenosine 5′-triphosphate (ATP) is an agonist for the P2Z receptor of human leukaemic lymphocytes and opens a Ca <sup>2+</sup>-selective ion channel, which also conducts Ba<sup>2+</sup>, Sr<sup>2+</sup> and the small fluorescent dye, ethidium<sup>+</sup>. A wide range of receptor agonists, many of which raise cytosolic [Ca<sup>2+</sup>] activate phospholipase D (PLD). In the present study, it was shown that both ATP and 3′-O-(4-benzoylbenzoyl)-ATP (BzATP) stimulated PLD activity in a concentration-dependent manner, and the inhibitory effects of suramin, oxidised ATP, extracellular Na<sup>+</sup> and Mg<sup>2+</sup> suggested that the effect of these agonists is mediated by P2Z receptors.
The role of divalent cations in ATP-stimulated PLD activity was investigated. Several agonists (eg ATP, thapsigargin, ionomycin) stimulated a rise in cytosolic [Ca<sup>2+</sup>] in human lymphocytes, but only ATP and ionomycin stimulated PLD activity. When Ca<sup>2+</sup> influx was prevented by EGTA, the majority of ATP-stimulated and all of ionomycin-stimulated PLD activity was inhibited. Preloading cells with the Ca<sup>2+</sup> chelator, BAPTA, reduced cytosolic [Ca<sup>2+</sup>] and, paradoxically, ATP-stimulated PLD activity was potentiated. ATP-stimulated PLD activity was supported by both Ba<sup>2+</sup> and Sr<sup>2+</sup> when they were substituted for extracellular Ca<sup>2+</sup>. Furthermore, both ATP-stimulated PLD activity and ATP-stimulated <sup>133</sup>Ba<sup>2+</sup> influx showed a linear dependence on extracellular [Ba<sup>2+</sup>]. Thus it was concluded that ATP stimulated PLD activity in direct proportion to the influx of divalent cations through the P2Z ion channel and this PLD activity was insensitive to changes in bulk cytosolic [Ca<sup>2+</sup>].
The calmodulin (Ca<sup>2+</sup>/CaM) inhibitor, trifluoperazine (TFP) inhibited ionomycin- and ATP-stimulated PLD activity and ATP-stimulated apoptosis, but had no effect on PLD activity already activated by ATP. However, TFP inhibited ATP-stimulated Ca<sup>2+</sup>, Ba<sup>2+</sup> and ethidium<sup>+</sup> fluxes, at concentrations below those which inhibit Ca<sup>2+</sup>/CaM, suggesting that TFP inhibits the P2Z receptor.
Similarly, the isoquinolinesulphonamide, KN-62, a selective inhibitor of Ca<sup>2+</sup>/CaM-dependent protein kinase II (CaMKII), also prevented ATP-stimulated apoptosis, but had no effect on pre-activated PLD. In addition, KN-62, and an analogue, KN-04, which has no effect on CaMKII, potently inhibited ATP-stimulated Ba<sup>2+</sup> influx (IC<sub>50</sub> 12.7 ± 1.5 and 17.3 ± 2.7 nM, respectively), ATP-stimulated ethidium<sup>+</sup> uptake (IC<sub>50</sub> 13.1 ± 2.6 and 37.2 ± 8.9 nM, respectively), ATP-stimulated phospholipase D activity (50% inhibition 5.9 ± 1.2 and 9.7 ± 2.8 nM, respectively) and ATP-induced shedding of the surface adhesion molecule, L-selectin (IC<sub>50</sub> 31.5 ± 4.5 and 78.7 ± 10.8 nM, respectively). They did not inhibit phorbol ester- or ionomycin-stimulated PLD activity or phorbol ester-induced L-selectin shedding. Neither KN-62 nor KN-04 (both 500 nM) have any effect on UTP-stimulated Ca<sup>2+</sup> transients in fura-2-loaded human neutrophils, a response which is mediated by the P2Y<sub>2</sub> receptor, neither did they inhibit ATP-stimulated contractile responses mediated by the P2X<sub>1</sub> receptor of guinea pig urinary bladder. Thus, KN-62 and KN-04 are almost equipotent as P2Z inhibitors with IC<sub>50</sub>s in the nanomolar, indicating that their actions cannot be due to CaMKII inhibition, but rather that they are potent and direct inhibitors of the P2Z receptor.
Extracellular ATP-induced shedding of L-selectin from lymphocytes into the medium is a Ca<sup>2+</sup>-independent response. L-selectin is either cleaved by a metalloproteinase or a PLD with specificity for glycosylphosphatidylinositol (GPI). The novel hydroxamic acid-based zinc chelator, Ro-31-9790 blocks ATP-induced L-selectin shedding, but was without effect on ATP-induced Ba<sup>2+</sup> influx or ATP-stimulated PLD activity. Furthermore, another zinc chelator, 1,10-phenanthroline, an inhibitor of a GPI-PLD, potentiated rather than inhibited ATP-stimulated PLD activity, suggesting that ATP-induced L-selectin shedding and ATP-stimulated PLD activity are independent of each other.
Although extracellular ATP is the natural ligand for the lymphocyte P2Z receptor, it is less potent than BzATP in stimulating Ba<sup>2+</sup> influx. Concentration-response curves for BzATP- and ATP-stimulated ethidium<sup>+</sup> influx gave EC<sub>50</sub>s 15.4 ± 1.4 µM and 85.6 ± 8.8 µM, respectively. The maximal response to ATP was only 69.8 ± 1.9% of that for BzATP. Hill coefficients were 3.17 ± 0.24 and 2.09 ± 0.45 for BzATP and ATP respectively, suggesting greater positive cooperativity for BzATP than for ATP in opening the P2Z-operated ion channel. A rank order of agonist potency of BzATP > ATP = 2MeSATP > ATPγS was observed for agonist-stimulated ethidium<sup>+</sup> influx, while maximal influxes followed a rank order of BzATP > ATP > 2MeSATP > ATPγS. When ATP (300 -1000 µM) was added simultaneously with 30 µM BzATP (EC<sub>90</sub>), it reduced both ethidium<sup>+</sup> and Ba<sup>2+</sup> fluxes by 30 - 40% relative to values observed with BzATP alone. KN-62, previously shown to be a specific inhibitor of the lymphocyte P2Z receptor, was a less potent antagonist of BzATP-induced fluxes than ATP, when maximal concentrations of both agonists (50 and 500 µM respectively) were used. However, when BzATP (18 µM) was used at a concentration equiactive with a maximally effective ATP concentration, KN-62 showed the same inhibitory potency for both agonists. The ecto-ATPase antagonist, ARL-67156, inhibited both ATP- and BzATP-stimulated Ba<sup>2+</sup> influx, suggesting that the lower efficacy of ATP compared with BzATP was not due to preferential hydrolysis of ATP. Thus, the natural ligand, ATP, is a partial agonist for the P2Z receptor while BzATP is a full agonist. Moreover the competitive studies show that only a single class of P2-receptor (P2Z class) is expressed on human leukaemic lymphocytes.
Both ATP- and BzATP-stimulated PLD activity were significantly inhibited (P < 0.05) when cells were suspended in iso-osmotic choline Cl medium. Choline<sup>+</sup> was found to be a permeant for the P2Z ion channel, since ATP induced a large uptake of [<sup>14</sup>C]choline<sup>+</sup> (60 to 150 µmol/ml intracellular water) during a 5 min incubation, which remained in the cells for several hours, and ATP was used to load cells with these levels of choline<sup>+</sup>. Intracellular choline<sup>+</sup> inhibited ATP-, BzATP-, PMA- and ionomycin-stimulated PLD activity. Brief exposure of lymphocytes to ATP increased the subsequent basal rate of ethidium<sup>+</sup> uptake, and this was prevented by intracellular choline<sup>+</sup>. It is proposed that P2Z-mediated Ca<sup>2+</sup> influx in lymphocytes activates PLD leading to significantly changes of the phospholipid composition of the plasma membrane, which subsequently produces a permeability lesion, which in turn contributes to cell death.
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Rouas-Freiss, Nathalie. "Présentation de l'antigène aux lymphocytes T : influence des phénomènes de capture de l'antigène." Paris 5, 1992. http://www.theses.fr/1992PA05P225.
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Mourade, Hélène. "Contribution à l'étude immunologique de l'infection chez le diabétique." Paris 5, 1990. http://www.theses.fr/1990PA05P157.
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Bich-Thuy, Lê Thi. "Mécanisme d'action de l'interleukine-2 dans l'activation, la prolifération et la différenciation des lymphocytes humains non activés par des agents exogènes." Lyon 1, 1987. http://www.theses.fr/1987LYO1H070.
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DiSanto, James Philip. "Molecular events in human T cell activation : CD4, CD8 and the human Lyt-3 molecules /." Access full-text from WCMC, 1989. http://proquest.umi.com/pqdweb?did=745024391&sid=1&Fmt=2&clientId=8424&RQT=309&VName=PQD.
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Debant, Marjolaine. "Etude de la dérégulation des entrées calciques du lymphocyte B de leucémie lymphoïde chronique : mise en évidence d'une nouvelle piste thérapeutique." Thesis, Brest, 2017. http://www.theses.fr/2017BRES0150.
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La leucémie lymphoïde chronique (LLC) constitue l'hémopathie maligne la plus fréquente dans les pays occidentaux et résulte d’une accumulation de lymphocytes B (LB) monoclonaux matures porteurs de la glycoprotéine CD5. Les LB de LLC sont également caractérisées par une altération de l'homéostasie du calcium avec, d'une part, la mise en évidence de facteurs de survie contrôlés par le calcium tels que phospho-ERK, NFAT-2 et IL-10, et d'autre part par une progression de la maladie qui est associée à la réponse au calcium. Tout d'abord, afin de mieux comprendre l'impact de la molécule CD5 sur les dérégulations du calcium, il a été montré que l'introduction d'un plasmide d'expression pour CD5 dans les lignées de cellules B humaines s'accompagnait d'une entrée calcique à l’état basale. Ensuite, cette entrée, appelée entrée constitutive, a été recherchée dans les LB de LLC pour montrer qu'elle caractérisait les patients non traités en phase d'évolution. Comme pour les lignées de cellules B CD5, cette nouvelle voie d'entrée du calcium est autonome et indépendante de la voie classique de signalisation du LB de LLC : BCR-IP3R. L'étude des protéines responsables de cet influx a permis de mettre en évidence, premièrement trois partenaires STIM1, Orai1 et TRPC1, et deuxièmement l'importance de la fraction membranaire de STIM1 (STIMPM) puisque l'utilisation d'un anticorps monoclonal anti-STIM1 (Acm) est capable d’inhiber l'entrée constitutive du calcium qui à son tour agit sur la survie des LB, pour les patients STIMPM positifs, lorsque l'Acm anti-STIM1 est utilisé en association avec le rituximab, un Acm thérapeutique anti-CD20. Enfin, la modélisation de la partie Cterminale de STIM1 permet d'envisager plusieurs cibles potentielles pour le développement de nouveaux Acm anti-STIM1. En conclusion, la mise en place, par le clone malin de LLC, d'une entrée constitutive du calcium favorise son agressivité et constitue donc une nouvelle voie thérapeutique contrôlable par l'utilisation d’Acm anti-STIM1 ce qui ouvre de nouvelles perspectives comme outils diagnostiques et thérapeutiques<br>Chronic lymphocytic leukemia (CLL) is the most common hematological malignancy in Western countries and is a result of the accumulation of mature monoclonal B lymphocytes (B-CLL) carrying the CD5 glycoprotein. The B-CLL are also characterized by an alteration of calcium homeostasis with, on the one hand, the demonstration of calcium-controlled survival factors such as phospho-ERK, NFAT- 2 and IL-10, and on the other hand by a progression of the disease which is associated with the response to calcium. Initially, in order to better understand the impact of the CD5 molecule on calcium deregulations, it has been shown that the introduction of an expression plasmid for CD5 into human B cell lines was accompanied by a calcium entry in the basal state. Then, this entry, called constitutive entry, was sought in the B-CLL to show that it characterized untreated patients in the evolution phase.As with CD5 B cell lines, this new calcium entry pathway is autonomous and independent of the classical B-CLL signaling pathway: BCR-IP3R. The study of the proteins responsible for this influx made it possible to highlight, firstly three partners (STIM1, Orai1 and TRPC1), and secondly the importance of the membrane fraction of STIM1 (STIMPM) since the use of a human monoclonal antibody (mAb) anti-STIM1 is able to inhibit the constitutive entry of calcium which in turn acts on the survival of B-CLL, for STIMPM positive patients, when the anti-STIM1 mAb was used in combination with rituximab, a therapeutic anti-CD20 mAb. Finally, the modeling of the C-terminal part of STIM1 makes it possible to envisage several potential targets for the development of new anti-STIM1 mAbs. In conclusion, the introduction by the CLL malignant clone of a constitutive entry of calcium favors its aggressiveness and thus constitutes a new therapeutic pathway controllable by the use of anti-STIM1 mAb, which opens new perspectives like diagnostic and therapeutic tools
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Kwan, Tin-fu. "Lymphocyte development in collagen-induced arthritis mice." Click to view the E-thesis via HKUTO, 2003. http://sunzi.lib.hku.hk/hkuto/record/B31971064.
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Krajewski, Andrew Stephen. "Human T-lymphocyte colony formation in vitro." Thesis, University of Edinburgh, 1985. http://hdl.handle.net/1842/24047.
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Boon, Adrianus Cornelis Maria. "Cytotoxic T lymphocyte-mediated immunity to influenza." [S.l.] : Rotterdam : [The Author] ; Erasmus University [Host], 2003. http://hdl.handle.net/1765/10473.
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Liu, Si. "B lymphocyte function in surgical anergic patients." Thesis, McGill University, 1988. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=64094.
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Hercus, Beth Justine. "Modelling T lymphocyte reactions to biomedical materials." Thesis, Queen Mary, University of London, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.423016.
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Harper, Catherine. "Studies of cytotoxic T-lymphocyte associated genes." Thesis, Brunel University, 1990. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.293103.
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