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Relevant bibliographies by topics / T cell activation; Unresponsiveness; Immunology

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Academic literature on the topic 'T cell activation; Unresponsiveness; Immunology'

Author: Grafiati

Published: 4 June 2021

Last updated: 3 February 2022

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Journal articles on the topic "T cell activation; Unresponsiveness; Immunology"

1

Ehl, Stephan, Winfried Barchet, Stephan Oehen, Peter Aichele, Joachim Hombach, Hans Hengartner, and Rolf M. Zinkernagel. "Donor cell persistence and activation-induced unresponsiveness of peripheral CD8+ T cells." European Journal of Immunology 30, no. 3 (March 2000): 883–91. http://dx.doi.org/10.1002/1521-4141(200003)30:3<883::aid-immu883>3.0.co;2-u.

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Rapoport, M. J., A. H. Lazarus, A. Jaramillo, E. Speck, and T. L. Delovitch. "Thymic T cell anergy in autoimmune nonobese diabetic mice is mediated by deficient T cell receptor regulation of the pathway of p21ras activation." Journal of Experimental Medicine 177, no. 4 (April 1, 1993): 1221–26. http://dx.doi.org/10.1084/jem.177.4.1221.

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Thymic T cell anergy, as manifested by thymocyte proliferative unresponsiveness to antigens expressed in the thymic environment, is commonly believed to mediate the acquisition of immunological self-tolerance. However, we previously found that thymic T cell anergy may lead to the breakdown of tolerance and predispose to autoimmunity in nonobese diabetic (NOD) mice. Here, we show that NOD thymic T cell anergy, as revealed by proliferative unresponsiveness in vitro after stimulation through the T cell receptor (TCR), is associated with defective TCR-mediated signal transduction along the PKC/p21ras/p42mapk pathway of T cell activation. PKC activity is reduced in NOD thymocytes. Activation of p21ras is deficient in quiescent and stimulated NOD T cells, and this is correlated with a significant reduction in the tyrosine phosphorylation of p42mapk, a serine/threonine kinase active downstream of p21ras. Treatment of NOD T cells with a phorbol ester not only enhances their p21ras activity and p42mapk tyrosine phosphorylation but also restores their proliferative responsiveness. Since p42mapk activity is required for progression through to S phase of the cell cycle, our data suggest that reduced tyrosine phosphorylation of p42mapk in stimulated NOD T cells may abrogate its activity and elicit the proliferative unresponsiveness of these cells.

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Hawiger, Daniel, Kayo Inaba, Yair Dorsett, Ming Guo, Karsten Mahnke, Miguel Rivera, Jeffrey V. Ravetch, Ralph M. Steinman, and Michel C. Nussenzweig. "Dendritic Cells Induce Peripheral T Cell Unresponsiveness under Steady State Conditions in Vivo." Journal of Experimental Medicine 194, no. 6 (September 17, 2001): 769–80. http://dx.doi.org/10.1084/jem.194.6.769.

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Dendritic cells (DCs) have the capacity to initiate immune responses, but it has been postulated that they may also be involved in inducing peripheral tolerance. To examine the function of DCs in the steady state we devised an antigen delivery system targeting these specialized antigen presenting cells in vivo using a monoclonal antibody to a DC-restricted endocytic receptor, DEC-205. Our experiments show that this route of antigen delivery to DCs is several orders of magnitude more efficient than free peptide in complete Freund's adjuvant (CFA) in inducing T cell activation and cell division. However, T cells activated by antigen delivered to DCs are not polarized to produce T helper type 1 cytokine interferon γ and the activation response is not sustained. Within 7 d the number of antigen-specific T cells is severely reduced, and the residual T cells become unresponsive to systemic challenge with antigen in CFA. Coinjection of the DC-targeted antigen and anti-CD40 agonistic antibody changes the outcome from tolerance to prolonged T cell activation and immunity. We conclude that in the absence of additional stimuli DCs induce transient antigen-specific T cell activation followed by T cell deletion and unresponsiveness.

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Barchet, Winfried, Jeffrey D. Price, Marina Cella, Marco Colonna, Sandra K. MacMillan, J. Perren Cobb, Paul A. Thompson, Kenneth M. Murphy, John P. Atkinson, and Claudia Kemper. "Complement-induced regulatory T cells suppress T-cell responses but allow for dendritic-cell maturation." Blood 107, no. 4 (February 15, 2006): 1497–504. http://dx.doi.org/10.1182/blood-2005-07-2951.

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Concurrent activation of the T-cell receptor (TCR) and complement regulator CD46 on human CD4+ T lymphocytes induces Tr1-like regulatory T cells that suppress through IL-10 secretion bystander T-cell proliferation. Here we show that, despite their IL-10 production, CD46-induced T-regulatory T cells (Tregs) do not suppress the activation/maturation of dendritic cells (DCs). DC maturation by complement/CD46-induced Tregs is mediated through simultaneous secretion of GM-CSF and soluble CD40L, factors favoring DC differentiation and reversing inhibitory effects of IL-10. Thus, CD46-induced Tregs produce a distinct cytokine profile that inhibits T-cell responses but leaves DC activation unimpaired. Such “DC-sparing” Tregs could be desirable at host/environment interfaces such as the gastrointestinal tract where their specific cytokine profile provides a mechanism that ensures unresponsiveness to commensal bacteria while maintaining reactivity to invading pathogens.

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Willems, F., F. Andris, D. Xu, D. Abramowicz, M. Wissing, M. Goldman, O. Leo, and H. Bazin. "The induction of human T cell unresponsiveness by soluble anti-CD3 mAb requires T cell activation." International Immunology 7, no. 10 (October 1, 1995): 1593–98. http://dx.doi.org/10.1093/intimm/7.10.1593.

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Pantaleo, G., D. Olive, A. Poggi, T. Pozzan, L. Moretta, and A. Moretta. "Antibody-induced modulation of the CD3/T cell receptor complex causes T cell refractoriness by inhibiting the early metabolic steps involved in T cell activation." Journal of Experimental Medicine 166, no. 2 (August 1, 1987): 619–24. http://dx.doi.org/10.1084/jem.166.2.619.

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We investigated the mechanism involved in T cell unresponsiveness that follows the monoclonal antibody-induced surface modulation of the CD3-TCR complex. We determined whether modulation of CD3-TCR affected the early metabolic steps such as [Ca2+]i rise and InsP3 formation. A strong inhibition of the increase on [Ca2+]i mediated by either anti-TCR or anti-CD2 mAbs was detected. In contrast, surface modulation of CD2 molecules did not prevent the [Ca2+]i increase induced by anti-TCR mAb. Similarly, InsP3 increase was strongly reduced only after modulation of CD3-TCR complex (but not of CD2 molecules). Therefore, it appears that surface modulation of CD3-TCR complex causes T cell refractoriness by inhibiting the very early metabolic events that follow receptor-ligand interactions.

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Jenkins, M. K., and R. H. Schwartz. "Antigen presentation by chemically modified splenocytes induces antigen-specific T cell unresponsiveness in vitro and in vivo." Journal of Experimental Medicine 165, no. 2 (February 1, 1987): 302–19. http://dx.doi.org/10.1084/jem.165.2.302.

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We investigated the antigen specificity and presentation requirements for inactivation of T lymphocytes in vitro and in vivo. In vitro studies revealed that splenocytes treated with the crosslinker 1-ethyl-3-(3-dimethylaminopropyl)-carbodiimide (ECDI) and soluble antigen fragments failed to stimulate significant proliferation by normal pigeon cytochrome c-specific T cell clones, suggesting that the chemical treatment inactivated full antigen presentation function. However, T cell clones exposed to ECDI-treated splenocytes and antigen in vitro were rendered unresponsive for at least 8 d to subsequent antigen stimulation with normal presenting cells. As predicted by the in vitro results, specific T cell unresponsiveness was also induced in vivo in B10.A mice injected intravenously with B10.A, but not B10.A(4R), splenocytes coupled with pigeon cytochrome c via ECDI. The antigen and MHC specificity of the induction of this T cell unresponsiveness in vitro and in vivo was identical to that required for T cell activation. These results suggest that nonmitogenic T cell recognition of antigen/MHC on ECDI-modified APCs results in the functional inactivation of T cell clones.

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Beyth, Shaul, Zipora Borovsky, Dror Mevorach, Meir Liebergall, Zulma Gazit, Hadi Aslan, Eithan Galun, and Jacob Rachmilewitz. "Human mesenchymal stem cells alter antigen-presenting cell maturation and induce T-cell unresponsiveness." Blood 105, no. 5 (March 1, 2005): 2214–19. http://dx.doi.org/10.1182/blood-2004-07-2921.

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AbstractInfusion of either embryonic or mesenchymal stem cells prolongs the survival of organ transplants derived from stem cell donors and prevents graft-versus-host-disease (GVHD). An in-depth mechanistic understanding of this tolerization phenomenon could lead to novel cell-based therapies for transplantation. Here we demonstrate that while human mesenchymal stem cells (hMSCs) can promote superantigen-induced activation of purified T cells, addition of antigen-presenting cells (APCs; either monocytes or dendritic cells) to the cultures inhibits the T-cell responses. This contact- and dose-dependent inhibition is accompanied by secretion of large quantities of interleukin (IL)–10 and aberrant APC maturation, which can be partially overridden by the addition of factors that promote APC maturation (ie, lipopolysaccharide [LPS] or anti-CD40 monoclonal antibody [mAb]). Thus, our data support an immunoregulatory mechanism wherein hMSCs inhibit T cells indirectly by contact-dependent induction of regulatory APCs with T-cell–suppressive properties. Our data may reveal a physiologic phenomenon whereby the development of a distinct APC population is regulated by the tissue's cellular microenvironment.

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Miller, G. T., P. S. Hochman, W. Meier, R. Tizard, S. A. Bixler, M. D. Rosa, and B. P. Wallner. "Specific interaction of lymphocyte function-associated antigen 3 with CD2 can inhibit T cell responses." Journal of Experimental Medicine 178, no. 1 (July 1, 1993): 211–22. http://dx.doi.org/10.1084/jem.178.1.211.

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Accessory cell surface molecules, such as T cell antigen CD2 and its ligand lymphocyte function-associated antigen 3 (LFA-3; CD58), are critical costimulatory pathways for optimal T cell activation in response to antigens. Interaction of CD2 with cell surface LFA-3 not only increases T cell/accessory cell adhesion, but also induces signal transduction events involved in the regulation of T cell responses. In this report, we show that specific interactions of LFA-3 with CD2 can result in T cell unresponsiveness to antigenic or mitogenic stimuli in vitro. By deletion of certain regions of the extracellular domain of LFA-3, we localized the CD2 binding site to the first domain of LFA-3. We then demonstrated that a soluble, purified first domain-LFA-3/IgG1 fusion protein (LFA3TIP) interacts with CD2 and binds to the same CD2 epitope as purified multimeric or cell surface-expressed LFA-3. LFA3TIP inhibits tetanus toxoid, hepatitis B surface antigen, anti-CD3 mAb, Con A, and phytohemagglutinin P-induced T cell proliferation, as well as xenogeneic and allogeneic mixed lymphocyte reactions (MLR). Unlike anti-LFA-3 or anti-CD2 monoclonal antibodies (mAbs) which inhibit T cell responses by blocking LFA-3/CD2 binding, LFA3TIP is capable of rendering T cells unresponsive to antigenic stimuli in situations where T cell activation is independent of CD2/LFA-3 interactions. Furthermore, LFA3TIP, but not blocking anti-CD2 mAbs, is capable of inducing T cell unresponsiveness to secondary stimulation in allogeneic MLR. This inhibition of T cell responses by LFA3TIP occurs through a different mechanism from that of mAbs to LFA-3 or CD2.

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Boucher, L. M., K. Wiegmann, A. Fütterer, K. Pfeffer, T. Machleidt, S. Schütze, T. W. Mak, and M. Krönke. "CD28 signals through acidic sphingomyelinase." Journal of Experimental Medicine 181, no. 6 (June 1, 1995): 2059–68. http://dx.doi.org/10.1084/jem.181.6.2059.

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T cell receptor recognition of antigen can lead either to T lymphocyte differentiation and proliferation or to a state of unresponsiveness, which is dependent on whether appropriate costimulatory signals are provided to the mature T cell. We have investigated a novel intracellular signaling pathway provided by the costimulatory molecule CD28. CD28 engagement triggers the activation of an acidic sphingomyelinase (A-SMase), which results in the generation of ceramide, an important lipid messenger intermediate. A-SMase activation by CD28 occurred in resting as well as in activated primary T cells or leukemic Jurkat cells. In contrast, ligation of either CD3 or CD2 did not result in A-SMase activation. Overexpression of recombinant A-SMase in Jurkat T cells substituted for CD28 with regard to nuclear factor-kB activation. These data suggest that CD28 provides an important costimulatory signal by activation of an acidic sphingomyelinase pathway.

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Dissertations / Theses on the topic "T cell activation; Unresponsiveness; Immunology"

1

Rankin, Alasdair Menzies. "An investigation of CD28/B7 family binding interactions and costimulation, using immunoglobulin fusion proteins." Thesis, University of Oxford, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.360469.

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Friedman, Rachel Sharon. "Early T cell activation in the lymphoid milieu." Diss., Search in ProQuest Dissertations & Theses. UC Only, 2007. http://gateway.proquest.com/openurl?url_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:dissertation&res_dat=xri:pqdiss&rft_dat=xri:pqdiss:3251945.

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Thesis (Ph.D.)--University of California, San Francisco, 2007.
Source: Dissertation Abstracts International, Volume: 68-02, Section: B, page: 0876. Adviser: Matthew F. Krummel. Includes supplementary digital materials.

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Moldovan, Maria-Cristina. "Role of CD4 dimerization in T cell activation." Thesis, McGill University, 2003. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=82936.

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Key to development of immunotherapies and vaccines is a thorough understanding of the complex pathways that govern T cell activation. On helper T lymphocytes, the CD4 molecule is a critical player in the early stages of activation, serving to enhance recognition of MHC-peptide complexes by the TcR and to facilitate efficient p56lck recruitment in the vicinity of the engaged TcR:CD3 signalling module. Originally, the CD4 molecule was believed to exist as a monomer on the cell surface; however, within the last years, a growing body of crystallographic, computer modeling and functional studies has suggested that CD4 might assume a dimeric/oligomeric state.
Here, we provide direct experimental evidence for the existence of CD4 dimers on the surface of transfected cells from haematopoietic and fibroblastic origin, as well as in primary T lymphocytes. Furthermore, we accurately map the dimerization site at residues K318 and Q344 within the fourth extracellular domain of CD4. More importantly, we demonstrate that dimer formation is essential for the coligand and coreceptor functions of CD4 in T cell activation. Specifically, we show that CD4 dimerization is required for efficient IL-2 production, yet appears without effect on early TcR-associated signalling. Using FRET video microscopy to visualize the dynamics of CD4 molecules during T cell activation, we reveal that CD4 dimers only promote immunological synapse formation, then further accumulate within the synapse.
Overall, the study presented in this thesis sheds light on the refined molecular interplay of the various surface receptors and signalling modules that dictates the efficiency of the T lymphocyte antigenic response.

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Poudrier, Johanne. "Contact events in T help for B cell activation." Thesis, McGill University, 1994. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=28517.

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The generation of an Ab response is modulated by contact and cytokine mediated T help for B cells. Here we show that murine splenic small resting B cells do not express mRNA for, or bear IL-2R. Accordingly, these cells do not respond to IL-2. T- contact events induce IL-2R expression on B cells and this is inhibited by blocking of CD40, MHC II or CD54. Although CD40 ligation on its own induces B cell proliferation, it does not confer IL-2 responsiveness. In contrast, signalling through MHC II and CD54 synergizes with IL-5 to induce functional IL-2R on B cells. Moreover, physiological, gp39$ rm sp{low},$ T help for B cell IL-2 responsiveness is equivalently dependent on ligation of CD40, CD54 and MHC II, and requires prior sIg signalling. IL-5 synergizes with either LPS or Th to render B cell responses to IL-2 autonomous of further stimulus. Thus, expression of a functional IL-2R is a marker of B cell activation which appears to be tightly regulated through sIg signals and T-contact events and can be modulated by cytokines.

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Krakowski, Michelle L. "T cell activation and cytokine production in experimental allergic encephalomyelitis." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape11/PQDD_0001/NQ44479.pdf.

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Bonnard, Madeleine. "A novel role for CD4 in antigen-mediated T-cell activation /." Thesis, McGill University, 1993. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=68156.

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A number of T-cell membrane molecules influence the outcome of antigen recognition by TCR/CD3 complex. CD4, by virtue of its non-covalent association with the protein tyrosine kinase lck has the capacity to enhance TCR$ alpha beta$ signalling. The extracellular domain of CD4 interacts with monomorphic determinants of Major Histocompatibility complex class-II molecules such that antigen presented in association with MHC class-II to CD4$ sp+$ T-cells results in the coaggregation of CD4 and TCR/CD3, thus juxtaposing lck and the antigen-receptor complex. Anti-CD4 antibodies abrogate both antigen and anti-TCR-induced T-cell activation. Studies using antigen specific T-cell clones that express either no CD4, wild type CD4 or mutated CD4 that cannot associate with lck (Db CYS) indicate that CD4 sequesters the majority of cellular lck and when not coaggregated with TCR/CD3, prevents the generation of prerequisite signals.
Results presented in this thesis indicate that while CD4-associated lck is providing prerequisite signals for TCR/CD3 signalling, the contribution of CD4 must be more than simply providing a shuttle for lck. Specifically, anti-CD4 inhibits the antigen response of Db CYS CD4-expressing clones. This result cannot be accounted for either by CD4 sequestration of lck, or reduction of avidity of the interaction between the T-cell and the antigen presenting cell, since CD4$ sp-$ variants exhibit an antigen response comparable to that of CD4$ sp+$ variants. Rather, they suggest a novel role for the ectodomain of CD4 in antigen-induced T-cell activation.

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Dushek, Omer. "Mathematical modeling in cellular immunology: T cell activation and parameter estimation." Thesis, University of British Columbia, 2008. http://hdl.handle.net/2429/2894.

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A critical step in mounting an immune response is antigen recognition by T cells. This step proceeds by productive interactions between T cell receptors (TCR) on the surface of T cells and foreign antigen, in the form of peptide-major-histocompatibility-complexes (pMHC), on the surface of antigen-presenting-cells (APC). Antigen recognition is exceedingly difficult to understand because the vast majority of pMHC on APCs are derived from self-proteins. Nevertheless, T cells have been shown to be exquisitely sensitive, responding to as few as 10 antigenic pMHC in an ocean of tens of thousands of self pMHC. In addition, T cells are extremely specific and respond only to a small subset of pMHC by virtue of their specific TCR. To explain the sensitivity of T cells to pMHC it has been proposed that a single pMHC may serially bind multiple TCRs. Integrating present knowledge on the spatial-temporal dynamics of TCR/pMHC in the T cell-APC contact interface, we have constructed mathematical models to investigate the degree of TCR serial engagements by pMHC. In addition to reactions within clusters, the models capture the formation and mobility of TCR clusters. We find that a single pMHC serially binds a substantial number of TCRs in a TCR cluster only if the TCR/pMHC bond is stabilized by coreceptors and/or pMHC dimerization. In a separate study we propose that serial engagements can explain T cell specificity. Using Monte Carlo simulations, we show that the stochastic nature of TCR/pMHC interactions means that multiple binding events are needed for accurate detection of foreign pMHC. Critical to our studies are estimates of TCR/pMHC reaction rates and mobilities. In the second half of the thesis, we show that Fluorescence Recovery After Photobleaching (FRAP) experiments can reveal effective diffusion coefficients. We then show, using asymptotic analysis and model fitting, that FRAP experiments can be used to estimate reaction rates between cell surface proteins, like TCR/pMHC. Lastly, we use FRAP experiments to investigate how the actin cytoskeleton modulates TCR mobility and report effective reaction rates between TCR and the cytoskeleton.

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Morgan, Sara Hannah. "Molecular aspects of antibody mediated T cell activation." Thesis, University of Oxford, 2009. http://ora.ox.ac.uk/objects/uuid:8c30ca07-b93b-46a7-aa86-01f94ee97e97.

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The normal physiological activation of naive T cells requires the engagement of both the T cell receptor (TCR) and the co-stimulatory molecule, CD28. However, a group of monoclonal antibodies (mAbs) have been identiﬁed that are able to activate T cells in vitro and in vivo via CD28 engagement alone. Two deﬁning characteristics found in all CD28 superagonist mAbs are their membrane proximal CD28 epitopes and the requirement for mAb immobilisation. To investigate whether agonistic mAbs to similar cell molecules could be identiﬁed based on epitope position alone, mAbs to the inhibitory receptor PD-1 were generated and characterised. Using a drastic mutation-based epitope mapping technique, one mAb was identiﬁed with a membrane proximal epitope along with two other mAbs with membrane distal epitopes. These mAbs were tested for triggering activity in a hybridoma stimulation assay. mAb stimulation was observed with all three mAbs but only in cells expressing a PD-1 chimera that associated with the TCR and the strength of activation was dependent on epitope location. Cross-linking of a monomeric PD-1/CD28 chimera with a pair of anti-PD-1 mAbs resulted in signalling in this system, however, suggesting a role for ligand aggregation in addition to epitope position in mAb signalling. To further investigate the role of epitope position in CD28 superagonism, a cell line expressing a chimeric form of CD28 was created wherein the superagonistic mAb epitope was moved to a membrane distal position. When stimulated with a CD28 superagonist mAb signalling was no longer observed. However stimulation with another mAb that had an epitope to a membrane proximal location on the chimera resulted in superagonistic effect. These results show that epitope location is the dominant cause of T cell stimulation observed by CD28 superagonist mAbs and that epitope dependent mAb signalling is possible in other T cell surface molecules. The work described in this thesis has implications for both the development of immune modulating mAb therapeutics and for the general mechanism of triggering of cell surface receptors dependent on extrinsic tyrosine kinases.

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Sabbagh, Laurent. "Transcriptional regulation of the murine caspase-3 gene during T cell activation." Thesis, McGill University, 2004. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=84320.

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Caspases play an important role in shaping the developing organism. They are required to eliminate unwanted or damaged cells and therefore are able to prevent disease. Several reports have shown increased caspase-3 expression in different cell types undergoing apoptosis. We undertook to examine the role of T cell activation through the T cell receptor (TCR) in regulating caspase-3 gene expression. The KOX-14 murine T cell hybridoma was initially used as a model for activation-induced cell death. Caspase-3 mRNA levels increased by 3-fold following T cell activation and was independent of STAT1 activation and therefore of IFN-gamma signaling in KOX-14 cells suggesting that the increase occurs early during T cell activation. Naive T cells were then isolated from the lymph nodes of mice to determine the extent of the increase in caspase-3 mRNA levels in cells undergoing proliferation rather than apoptosis. Caspase-3 mRNA levels were selectively induced (13-fold) following TCR triggering. Furthermore, caspase-3 mRNA levels were the highest in effector T cells which are destined to undergo AICD, when compared to long-lived memory T cells. Interestingly, the levels of procaspase-3 were also induced (6-fold) in activated peripheral T cells. In addition, T cells deficient for caspase-3 were more resistant to different apoptosis inducing molecules when compared to T cells containing normal levels of caspase-3. Altogether, these results demonstrate that the levels of caspase-3 must be maintained in a cell to ensure efficient apoptosis. The caspase-3 promoter region was subsequently cloned to identify transcription factors responsible for the observed increased in caspase-3 mRNA levels during T cell activation. Several regions within the promoter had either positive or negative regulatory effects on reporter activity when deleted. TCR stimulation of KOX-14 cells containing the different caspase-3 promoter constructs did not show changes in reporter ac

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Clement, Mathew. "The role of the CD8 co-receptor in CD8+ T-cell activation." Thesis, Cardiff University, 2013. http://orca.cf.ac.uk/47019/.

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CD8+ T-cells are essential for the immune control of pathogens and the natural eradication of cancer. CD8+ T-cells also play a major role in the pathogenesis of autoimmunity and alloreactivity. CD8+ T-cells recognize short peptide fragments (8-13 amino acids) presented at the target cell surface bound to Major Histocompatability Class I (MHCI) molecules. Tcell antigen recognition is unique in nature because it involves the binding of a single ligand (peptide–MHC [pMHC]) by two receptors (TCR and CD8). The CD8 glycoprotein, which serves as the coreceptor on MHCI-restricted T-cells, acts to enhance the antigen sensitivity of T-cells by binding to a largely invariant region of MHCI at a site distinct from the TCR docking platform. CD8 has been shown to have multiple roles including enhancing effects on early T-cell activation events and also in controlling the level of T-cell cross-reactivity. The pMHCI/CD8 interaction is classified as having a very weak binding affinity and very fast kinetics. I discovered that this low solution binding affinity is essential in maintaining homeostasis as dramatically increasing the strength of this interaction resulted in total loss of T-cell specificity and activation independent of TCR engagement. This led me to examine the possibility that anti-CD8 antibodies could also bypass the normal requirements for T-cell activation. I identified one specific clonotype of antibody capable of this phenomenon but simultaneously discovered multiple effector phenotypes of other anti-CD8 antibodies. These included both enhancing and inhibitory effects on pMHCI tetramer binding and CD8+ T-cell activation. Subsequently, I explored the possibility of using these inhibitory anti-CD8 antibodies to block T-cell function in systems which are highly dependent on CD8 such as autoreactive CD8+ T-cells. I demonstrated that targeting CD8 can be used as a strategy to block autoreactive CD8+ T-cell activation in the absence of any effect on pathogen specific immunity. This highlights a novel therapeutic strategy that warrants further investigation. Finally, I demonstrated that CD8 can alter the functional avidity of a CD8+ T-cell for its agonists and act to re-arrange the relative potencies of each of its potential agonists, a novel “focussing mechanism” for CD8 in T cell activation. These results provide new insight to the biological role of CD8 in T-cells and even predict a novel mechanism for CD8 in controlling T-cell function. My results also highlight the potential of targeting CD8 for immunotherapeutic design in autoimmune disorders.

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Books on the topic "T cell activation; Unresponsiveness; Immunology"

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Miami Bio/Technology Winter Symposium (1990 Miami, Fla.). Advances in gene technology: The molecular biology of immune diseases and the immune reponse : proceedings of the 1990 Miami Bio/Technology Winter Symposia. Oxford: IRL Press, 1990.

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Charles, Snow E., ed. T-cell dependent and independent B-cell activation. Boca Raton: CRC Press, 1991.

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Branch, Moody D., ed. T cell activation by CD1 and lipid antigens. Berlin: Springer, 2007.

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T Cell Activation by CD1 and Lipid Antigens (Current Topics in Microbiology and Immunology Book 314). Springer, 2007.

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Jean-Marie, Andrieu, Lu Wei, and International Symposium on Cellular Approaches to the Control of HIV Disease (1st : 1994 : Paris, France), eds. Cell activation and apoptosis in HIV infection: Implications for pathogenesis and therapy. New York: Plenum Press, 1995.

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Feldmann, M., and R. Maini. T-Cell Activation in Health and Disease Disorders of Immune Regulation Infection and Autoimmunity: Papers from an International Meeting in Oxford, U. Academic Press, 1989.

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(Editor), Jean-Marie Andrieu, and Wei Lu (Editor), eds. Cell Activation and Apoptosis in HIV Infection: Implications for Pathogenesis and Therapy (Advances in Experimental Medicine and Biology). Springer, 1995.

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T-cell activation in health and disease: Disorders of immune regulation : infection and autoimmunity : papers from an international meeting in Oxford, UK, in September 1988. London: Academic Press, 1989.

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Marc, Feldmann, Maini R. N, Woody James N, and United States. Naval Medical Research and Development Command., eds. T-cell activation in health and disease: Disorders of immune regulation infection and autoimmunity : papers from an international meeting in Oxford, UK, in September 1988. London ; San Diego: Academic Press, 1989.

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Hartigan-O’Connor, Dennis J., and Christian Brander. Immunology. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190493097.003.0005.

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The key factor in HIV pathogenesis is the decline in CD4+ T cells with resultant immunodeficiency and chronic inflammation. Depletion of CD4+ T cells from the gastrointestinal mucosa followed by microbial translocation and subsequent immune activation are components of disease progression in untreated patients. Symptomatic and occult opportunistic infections including cytomegalovirus contribute to chronic inflammation in persons infected with HIV. Antiretroviral therapy (ART) results in immune reconstitution, with increases in peripheral CD4+ T cell lymphocytes in most persons infected with HIV, although immune recovery is quite variable. A subset of patients with AIDS will develop immune reconstitution inflammatory syndromes after initiation of ART. Approximately 1% of persons with HIV are able to control infection without the need for ART (“elite” controllers). A variety of immune-based therapies, including hydroxyurea, growth hormone, and statins, are being studied in clinical trials and may ultimately play a role in treating persons with HIV infection.

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Book chapters on the topic "T cell activation; Unresponsiveness; Immunology"

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Pier, Gerald B., Howard Ceri, Chris Mody, and Michael Preston. "T-Cell Maturation and Activation." In Immunology, Infection, and Immunity, 315–42. Washington, DC, USA: ASM Press, 2015. http://dx.doi.org/10.1128/9781555816148.ch14.

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Kaufman, M., F. Andris, and O. Leo. "Theoretical Insight into Antigen-Induced T-Cell Unresponsiveness." In Theoretical and Experimental Insights into Immunology, 93–115. Berlin, Heidelberg: Springer Berlin Heidelberg, 1992. http://dx.doi.org/10.1007/978-3-642-76977-1_7.

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Bertolino, Patrick, and David G. Bowen. "Primary T-Cell Activation in Liver." In Encyclopedia of Medical Immunology, 899–905. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-0-387-84828-0_65.

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McNally, J. M., and R. M. Welsh. "Bystander T Cell Activation and Attrition." In Current Topics in Microbiology and Immunology, 29–41. Berlin, Heidelberg: Springer Berlin Heidelberg, 2002. http://dx.doi.org/10.1007/978-3-642-56055-2_3.

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Trendel, Nicola C., and Omer Dushek. "Mathematical Modelling of T Cell Activation." In Mathematical, Computational and Experimental T Cell Immunology, 223–40. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-57204-4_13.

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Hünig, T., G. Tiefenthaler, E. Schlipköter, and A. Lawetzky. "The T-Cell Antigen Receptor and CD2 in Rat T-Cell Activation and Ontogeny." In Progress in Immunology, 139–46. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-83755-5_19.

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Arstila, T. P. "T Cell Subsets and the Activation of γδ T Cells." In Current Topics in Microbiology and Immunology, 71–77. Berlin, Heidelberg: Springer Berlin Heidelberg, 1996. http://dx.doi.org/10.1007/978-3-642-80057-3_7.

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Schreiber, R. D., E. R. Unanue, and G. J. Bancroft. "T Cell-Independent Macrophage Activation in Scid Mice." In Current Topics in Microbiology and Immunology, 235–42. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-74974-2_28.

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Goodwin, J. S. "Regulation of T-Cell Activation by Leukotriene B4." In Lipid Mediators in the Immunology of Shock, 469–81. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4613-0919-2_51.

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Burakoff, S. J., T. Collins, W. C. Hahn, J. K. Park, B. P. Sleckmann, V. Igras, Y. Rosenstein, and B. E. Bierer. "The Role of Co-receptors in T Cell Activation." In Progress in Immunology Vol. VIII, 275–81. Berlin, Heidelberg: Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-642-51479-1_36.

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Conference papers on the topic "T cell activation; Unresponsiveness; Immunology"

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Smith, Peter L., and A. G. Dalgleish. "Abstract B13: Immunogenic chemotherapy alters microbiome-induced T-cell activation." In Abstracts: AACR Special Conference on Tumor Immunology and Immunotherapy; November 17-20, 2019; Boston, MA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/2326-6074.tumimm19-b13.

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Dong, Shilan, Jason Cahoon, Tasnim Khalifa, and Rachit Ohri. "Abstract A74: T cell activation standardization for therapeutic assay development." In Abstracts: AACR Special Conference on Tumor Immunology and Immunotherapy; October 1-4, 2017; Boston, MA. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/2326-6074.tumimm17-a74.

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Singer, Meromit, Chao Wang, Le Cong, Nemanja D. Marjanovic, Monika S. Kowalczyk, Huiyuan Zhang, Jackson Nyman, et al. "Abstract A10: A distinct gene module for T cell dysfunction uncoupled from T cell activation and controlled by metallothioneins." In Abstracts: AACR Special Conference on Tumor Immunology and Immunotherapy; October 20-23, 2016; Boston, MA. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/2326-6074.tumimm16-a10.

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Grimster, Neil, Lisa Drew, Stephen Fawell, Deanna A. Mele, Gayathri Bommakanti, Minhui Shen, Kevin Xu, et al. "Abstract A56: Releasing the brake on T-cell activation through inhibition of HPK1." In Abstracts: AACR Special Conference on Tumor Immunology and Immunotherapy; November 17-20, 2019; Boston, MA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/2326-6074.tumimm19-a56.

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Wesa, Amy, Yumei Xiong, Tim Chan, Jeff Rosenbloom, Srinivas Rengarajan, Paul Szymanski, John A. Barrett, Francois Lebel, Farzad Haerizadeh, and Richard Einstein. "Abstract B25: Controlled production of a bispecific antibody by a genetically modified stem cell triggers T cell activation and cytolysis in non-small cell lung carcinoma." In Abstracts: AACR Special Conference: Tumor Immunology and Immunotherapy: A New Chapter; December 1-4, 2014; Orlando, FL. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/2326-6074.tumimm14-b25.

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Wang, Liang-Chuan S., Albert Lo, John Scholler, Carl H. June, Ellen Pure, and Steven M. Albelda. "Abstract PR14: Fibroblast activation protein as a universal target for chimeric antigen receptor T cell therapy in solid tumors." In Abstracts: AACR Special Conference on Tumor Immunology: Multidisciplinary Science Driving Basic and Clinical Advances; December 2-5, 2012; Miami, FL. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.tumimm2012-pr14.

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Eruslanov, Evgeniy, Pratik Bhojnagarwala, Jon Quatromoni, Tom Stephen, Anjana Ranganathan, Charuhas Deshpande, Tatiana Akimova, et al. "Abstract A66: Tumor-associated neutrophils in early stage human lung cancer are not immunosuppressive, but exhibit an inflammatory phenotype and provide accessory signals for T cell activation." In Abstracts: AACR Special Conference: Tumor Immunology and Immunotherapy: A New Chapter; December 1-4, 2014; Orlando, FL. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/2326-6074.tumimm14-a66.

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Lazorchak, Adam S., Troy Patterson, Yueyun Ding, Pottayil G. Sasikumar, Naremaddepalli S. Sudarshan, Nagaraj M. Gowda, Raghuveer K. Ramachandra, et al. "Abstract A36: CA-170, an oral small molecule PD-L1 and VISTA immune checkpoint antagonist, promotes T cell immune activation and inhibits tumor growth in pre-clinical models of cancer." In Abstracts: AACR Special Conference on Tumor Immunology and Immunotherapy; October 20-23, 2016; Boston, MA. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/2326-6074.tumimm16-a36.

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