Relevant bibliographies by topics / T cell activation/tolerance

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'T cell activation/tolerance'

Author: Grafiati
Published: 18 May 2024

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Journal articles on the topic "T cell activation/tolerance"

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Priyadharshini, Bhavana, Dale L. Greiner, and Michael A. Brehm. "T-cell activation and transplantation tolerance." Transplantation Reviews 26, no. 3 (July 2012): 212–22. http://dx.doi.org/10.1016/j.trre.2011.09.002.

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Phillips, J. A., C. G. Romball, M. V. Hobbs, D. N. Ernst, L. Shultz, and W. O. Weigle. "CD4+ T cell activation and tolerance induction in B cell knockout mice." Journal of Experimental Medicine 183, no. 4 (April 1, 1996): 1339–44. http://dx.doi.org/10.1084/jem.183.4.1339.

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B cell knockout mice microMT/microMT were used to examine the requirement for B cell antigen (Ag) presentation in the establishment of CD4+ T cell tolerance. CD4+T cells from microMT mice injected with exogenous protein Ag in adjuvant responded to in vitro challenge by transcription of cytokine mRNA, cytokine secretion, and proliferation. Peripheral tolerance could be established in microMT mice with a single dose of deaggragated protein. This tolerance was manifested by a loss of T cell proliferation and cytokine production (including both T helper cell type 1 [Th1]- and Th2-related cytokines), indicating that B cells are not required for the induction of peripheral T cell tolerance and suggesting that the dual zone tolerance theory is not applicable to all protein Ags and is not mediated through Ag presentation by B cells.
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Jonuleit, Helmut, Edgar Schmitt, Hacer Kakirman, Michael Stassen, Jürgen Knop, and Alexander H. Enk. "Infectious Tolerance." Journal of Experimental Medicine 196, no. 2 (July 15, 2002): 255–60. http://dx.doi.org/10.1084/jem.20020394.

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Regulatory CD4+CD25+ T cells (Treg) are mandatory for maintaining immunologic self-tolerance. We demonstrate that the cell-cell contact–mediated suppression of conventional CD4+ T cells by human CD25+ Treg cells is fixation resistant, independent from membrane-bound TGF-β but requires activation and protein synthesis of CD25+ Treg cells. Coactivation of CD25+ Treg cells with Treg cell–depleted CD4+ T cells results in anergized CD4+ T cells that in turn inhibit the activation of conventional, freshly isolated CD4+ T helper (Th) cells. This infectious suppressive activity, transferred from CD25+ Treg cells via cell contact, is cell contact–independent and partially mediated by soluble transforming growth factor (TGF)-β. The induction of suppressive properties in conventional CD4+ Th cells represents a mechanism underlying the phenomenon of infectious tolerance. This explains previously published conflicting data on the role of TGF-β in CD25+ Treg cell–induced immunosuppression.
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Dowling, Samuel Dae, Enric Mocholi, Ross Gruber, Bridget Shafit-Zagardo, and Fernando Macian. "Macroautophagy regulates T helper cell activation and tolerance." Journal of Immunology 196, no. 1_Supplement (May 1, 2016): 56.10. http://dx.doi.org/10.4049/jimmunol.196.supp.56.10.

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Abstract Macroautophagy is a catabolic process whereby cell components, which range from soluble proteins to whole organelles, are sequestered in de novo formed double-membrane autophagosomes that fuse with lysosomes to degrade their cargo. Effector T helper cells induce macroautophagy during activation to maintain cell proliferation and cytokine production. T cells that are unable to upregulate macroautophagy activity show a reduction in ATP generation, suggesting that macroautophagy is necessary to maintain the energy metabolism required to meet the demands of T cell activation. It is presently unknown whether macroautophagy regulates the activation state and functional capacity of CD4+T cells. We explored the instructive role of macroautophagy in effector T helper cell activation and tolerance. Inhibition of macroautophagy during activation of CD4+T helper type 1 (TH1) cells induces a long-lasting state of hyporesponsiveness, with a molecular signature that resembles that of anergic T cells. Moreover, inhibition of macroautophagy prevented activated TH1 cells from upregulating glycolysis and mitochondrial respiration, supporting that macroautophagy may regulate metabolic homeostasis during activation of effector T helper cells. Consequently, inhibition of macroautophagy in vivo prevents CD4+ T cell activation in response to immunization and results in decreased severity of experimental autoimmune encephalomyelitis. Our data support that macroautophagy, likely by regulating metabolism, is necessary for the activation of effector T helper cells and that its absence induces a tolerant state.
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Abbas, Abul K. "The control of T cell activation vs. tolerance." Autoimmunity Reviews 2, no. 3 (May 2003): 115–18. http://dx.doi.org/10.1016/s1568-9972(03)00028-4.

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Mondino, A., A. Khoruts, and M. K. Jenkins. "The anatomy of T-cell activation and tolerance." Proceedings of the National Academy of Sciences 93, no. 6 (March 19, 1996): 2245–52. http://dx.doi.org/10.1073/pnas.93.6.2245.

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Nurieva, Roza, Guillermina Lozano, and Chen Dong. "Regulation of naïve T cell tolerance and regulatory T cell function by GRAIL (113.21)." Journal of Immunology 186, no. 1_Supplement (April 1, 2011): 113.21. http://dx.doi.org/10.4049/jimmunol.186.supp.113.21.

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Abstract CD4+ T cells are the master regulators of adaptive immune responses, and many autoimmune diseases arise due to a breakdown of self tolerance in CD4+ cells. Gene related to anergy in lymphocytes (GRAIL), the E3 ubiqutine ligase, has acknowledged as one of key molecules implicated in T cell activation and tolerance. In order to understand the physiological function of GRAIL in immune regulation, we have generated and analyzed GRAIL deficient mice. Naive T cells lacking GRAIL showed greatly enhanced proliferation and cytokine production after T cell receptor (TcR) activation. In addition, lack of GRAIL abrogated suppressive function of regulatory T (Treg) cells. We found that GRAIL deficient naive and Treg cells after TcR activation expressed substantially higher amounts of NFATc1 compared to wild-type cells, whereas the activation of other factors in AP-1 and NFκB pathways were normal. Our data also suggested that sustained TcR cell-surface expression in the absence of GRAIL led to selective NFATc1 expression in both naive T cells and Treg cells. In contrast to naïve T cells, GRAIL, through controlling NFATc1 expression, inhibits IL-21 production and upregulation of Th17-specific genes in Treg cells. Thus, the immune regulation by GRAIL in both naive and Treg cells is absolutely critical as evidenced by the failure of T cell tolerance induction and greatly increased susceptibility to autoimmune diseases of GRAIL deficient mice.
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Berg-Brown, Nancy N., Matthew A. Gronski, Russell G. Jones, Alisha R. Elford, Elissa K. Deenick, Bernhard Odermatt, Dan R. Littman, and Pamela S. Ohashi. "PKCθ Signals Activation versus Tolerance In Vivo." Journal of Experimental Medicine 199, no. 6 (March 15, 2004): 743–52. http://dx.doi.org/10.1084/jem.20031022.

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Understanding the pathways that signal T cell tolerance versus activation is key to regulating immunity. Previous studies have linked CD28 and protein kinase C-θ (PKCθ) as a potential signaling pathway that influences T cell activation. Therefore, we have compared the responses of T cells deficient for CD28 and PKCθ in vivo and in vitro. Here, we demonstrate that the absence of PKCθ leads to the induction of T cell anergy, with a phenotype that is comparable to the absence of CD28. Further experiments examined whether PKCθ triggered other CD28-dependent responses. Our data show that CD4 T cell–B cell cooperation is dependent on CD28 but not PKCθ, whereas CD28 costimulatory signals that augment proliferation can be uncoupled from signals that regulate anergy. Therefore, PKCθ relays a defined subset of CD28 signals during T cell activation and is critical for the induction of activation versus tolerance in vivo.
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Lechler, Robert, Jian-Guo Chai, Federica Marelli-Berg, and Giovanna Lombardi. "T–cell anergy and peripheral T–cell tolerance." Philosophical Transactions of the Royal Society of London. Series B: Biological Sciences 356, no. 1409 (May 29, 2001): 625–37. http://dx.doi.org/10.1098/rstb.2001.0844.

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The discovery that T–cell recognition of antigen can have distinct outcomes has advanced understanding of peripheral T–cell tolerance, and opened up new possibilities in immunotherapy. Anergy is one such outcome, and results from partial T–cell activation. This can arise either due to subtle alteration of the antigen, leading to a lower–affinity cognate interaction, or due to a lack of adequate co–stimulation. The signalling defects in anergic T cells are partially defined, and suggest that T–cell receptor (TCR) proximal, as well as downstream defects negatively regulate the anergic T cell's ability to be activated. Most importantly, the use of TCR–transgenic mice has provided compelling evidence that anergy is an in vivo phenomenon, and not merely an in vitro artefact. These findings raise the question as to whether anergic T cells have any biological function. Studies in rodents and in man suggest that anergic T cells acquire regulatory properties; the regulatory effects of anergic T cells require cell to cell contact, and appear to be mediated by inhibition of antigen–presenting cell immunogenicity. Close similarities exist between anergic T cells, and the recently defined CD4 + CD25 + population of spontaneously arising regulatory cells that serve to inhibit autoimmunity in mice. Taken together, these findings suggest that a spectrum of regulatory T cells exists. At one end of the spectrum are cells, such as anergic and CD4 + CD25 + T cells, which regulate via cell–to–cell contact. At the other end of the spectrum are cells which secrete antiinflammatory cytokines such as interleukin 10 and transforming growth factor–β. The challenge is to devise strategies that reliably induce T–cell anergy in vivo , as a means of inhibiting immunity to allo– and autoantigens.
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Yu, Hong, Hiroshi Nishio, Joseph Barbi, Marisa Mitchell-Flack, Paolo Vignali, Ying Zheng, Andriana Lebid, et al. "The neurotrophic factor Neuritin regulates T cell anergy and T regulatory cell function." Journal of Immunology 208, no. 1_Supplement (May 1, 2022): 56.03. http://dx.doi.org/10.4049/jimmunol.208.supp.56.03.

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Abstract T cell activation and tolerance are tightly regulated to ensure effective elimination of foreign antigen while maintaining immune tolerance to self-antigens. Development of T cell anergy and regulatory T cell (Treg) mediated suppression both contribute to the establishment of immune tolerance. Here, we show that neuritin (Nrn1), a conserved GPI-anchored surface molecule important for the development, survival and function of neurons, is highly expressed in anergic and Treg cells. Nrn1 deficient CD4 cells are resistant to Treg cell mediated suppression, display defective anergy induction, and have reduced peripheral Treg generation. Nrn1 deficient Foxp3+ Treg cells exhibit reduced control of inflammatory colitis. Moreover, upon induction of experimental autoimmune encephalomyelitis (EAE), Nrn1 deficient mice develop non-remitting disease and have increased spinal cord inflammatory infiltrates. These in vivo findings underscore the importance of Nrn1 in immune tolerance. Recently, Nrn1 was identified as an accessory component of the ionotropic AMPA receptor (AMPAR) complex in neurons. AMPARs mediate glutamate dependent cation flux and regulate cell membrane potential. Cell membrane potential can impact nutrient uptake, calcium influx, cell size, proliferation and survival. In vitro analysis reveals that Nrn1 deficient Treg cells exhibit reduced proliferation and survival, associated with higher membrane potential, reduced nutrient sensitivity, reduced glycolysis and mTOR activation. AMPAR blockade can correct proliferation defect in Nrn1 deficient Treg cells. These findings reveal Nrn1 as an important regulator of immune tolerance functioning through the modulation of glutamate activated AMPAR.
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Dissertations / Theses on the topic "T cell activation/tolerance"

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Honey, Karen J. "Mechanisms of transplantation tolerance." Thesis, University of Oxford, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.301519.

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Chung, Chen-Yen. "CD4+ T cell responses to myelin autoantigens : activation, memory and tolerance." Thesis, University of Edinburgh, 2009. http://hdl.handle.net/1842/4013.

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Experimental autoimmune encephalomyelitis (EAE) is a CD4+ T cell mediated autoimmune disease of the central nervous system and shares many characteristics with multiple sclerosis (MS). Induction of EAE is mediated by myelin reactive CD4+ T helper (Th) cells, particularly Th1 and Th17 cells, which can be provoked by the immunization with myelin derived protein (or peptide) and Toll-like receptor (TLR) stimulus (eg, complete Freund¡s adjuvant, CFA). If given an injection of soluble peptide before immunization, mice do not develop EAE (they are tolerant). This approach has been widely applied, evoking tolerance in primary responses (i.e., in naive T cells). Therefore the first hypothesis of this thesis is that peptide induced protection from EAE is a result from T cell deletion or / and anergy. As MS patients have ongoing disease and over 85% of MS patients develop a relapsing-remitting course, memory T cells are key targets when considering peptide-induced tolerance as a therapeutic strategy. Thus, a model for ¡memory EAE¡ was established to test a second hypothesis that the myelin reactive memory T cells can be controlled by the administration of soluble peptide. Here, adoptive transfer of T cells from T cell receptor transgenic mice (2D2) recognizing myelin oligodendrocyte glycoprotein 35-55 (pMOG) was used to investigate the pMOG-reactive memory responses. Soluble pMOG administration could induce a transient expansion of 2D2 T cells followed by their loss through apoptosis. A model using double immunization was established by immunizing mice first with pMOG together with unmethylated CpG oligonucleotide (CpG) as an adjuvant, and subsequently immunizing with pMOG in CFA. This produced EAE with early onset and high incidence compared to mice which received pMOG/CFA only. Cells from mice that received the double immunization protocol produced high levels of IFN-γ, suggesting that memory T cell responses have been triggered in the mice. Administration of soluble peptide before secondary immunization could ameliorate EAE, indicating that memory T cells are susceptible to tolerance induction. pMOG-reactive memory T cells were further assessed by isolating CD4+ CD25- CD44high CD62Llow cells from pMOG-experienced 2D2 mice. These cells showed early and high production of IFN-γ, and early but transient production of IL-2, compared with naive population. These data provide basic information relevant to translating peptide-induced T cell tolerance from mice to humans.
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Erhardt, Annette. "Tolerance induction in the liver after T and NKT cell activation." kostenfrei, 2008. http://www.opus.ub.uni-erlangen.de/opus/volltexte/2008/1032/.

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Strainic, Michael George Jr. "THE ABSENCE OF C3AR AND C5AR SIGNAL TRANSDUCTION PROMOTES T REGULATORY CELL DIFFERENTIATION AND REGULATES IMMUNOLOGIC TOLERANCE." Case Western Reserve University School of Graduate Studies / OhioLINK, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=case1363707372.

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Seamons, Audrey. "Implications of myelin basic protein processing and presentation on T cell activation and tolerance /." Thesis, Connect to this title online; UW restricted, 2004. http://hdl.handle.net/1773/10851.

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Jangalwe, Sonal. "Regulation of Alloreactive CD8 T Cell Responses by Costimulation and Inflammation." eScholarship@UMMS, 2017. https://escholarship.umassmed.edu/gsbs_diss/907.

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CD8 T lymphocytes are a crucial component of the adaptive immune system and mediate control of infections and malignancy, but also autoimmunity and allograft rejection. Given their central role in the immune system, CD8 T cell responses are tightly regulated by costimulatory signals and cytokines. Strategies targeting signals that are critical for T cell activation have been employed in a transplantation setting to impede alloreactive T cell responses and prevent graft rejection. The goal of my thesis is to understand how costimulatory signals and inflammation regulate alloreactive CD8 T cell responses and how to target these pathways to develop more effective tools to prevent graft rejection. Costimulation blockade is an effective approach to prolong allograft survival in murine and non-human primate models of transplantation and is an attractive alternative to immunosuppressants. I describe a novel murine anti-CD40 monoclonal antibody that prolongs skin allograft survival across major histocompatibility barriers and attenuates alloreactive CD8 T cell responses. I find that the pro-apoptotic proteins Fas and Bim function concurrently to regulate peripheral tolerance induction to allografts. Activation of the innate immune system by endogenous moIecules released during surgery or infections in transplant recipients can modulate T cell responses. However, the direct impact of inflammation on alloreactive CD8 T cell responses is not clear. Using a T cell receptor (TCR) transgenic mouse modeI, I demonstrate that inflammatory stimuli bacterial lipopolysaccharide (LPS) and the viral dsRNA mimetic poly(I:C) differentially regulate donor-reactive CD8 T cell responses by generating distinct cytokine milieus. Finally I demonstrate the role of pro-inflammatory cytokines stem cell factor (SCF), granulocyte-macrophage colony-stimulating factor (GM-CSF) and interleukin-3 (IL-3) in improving human B cell development in humanized NOD-scid IL2Rγnull (NSG) mice.
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Schroder, Paul. "Targeting Signal 1 of T cell Activation to Restore Self Tolerance in Type 1 Diabetes." University of Toledo Health Science Campus / OhioLINK, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=mco1381086555.

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Kaye, P. M. J. "Particle mediated co-delivery of IL-10 and antigen inhibits T cell activation but fails to induce tolerance." Thesis, University College London (University of London), 2011. http://discovery.ucl.ac.uk/1302067/.

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Immune disorders such as allergy and autoimmunity are becoming increasingly common in developed countries. Self-reactive T cells exist in both healthy and autoimmune individuals. It is generally understood that hyperimmune disorders are caused by insufficient regulation, namely loss of activity of regulatory T cells. Whilst regulatory T cells exist naturally it is also possible to induce them both in vitro and in vivo. Immunotherapeutic techniques aim to provide noninflammatory exposure of antigen to the immune system with the aim of inducing antigen-specific regulatory T cells. Interleukin-10 (IL-10) is a cytokine with well known immunosuppressive qualities. It inhibits both the migration and the antigen-presenting ability of dendritic cells. It also has direct effects on T cells. Indeed, IL-10-secreting TR1 regulatory T cells were identified almost 15 years ago; their in vitro generation being dependent on exposure to IL-10. Particle-mediated DNA delivery (PMDD) is a promising method of immunisation and is especially suited to vaccines intended to have greater control over the response they induce. One of the main reasons for this is the possibility of including genes encoding immunomodulatory molecules alongside the antigen gene. This study utilises a mouse model involving the adoptive transfer of TCR-transgenic CD4+ T cells and establishes the response of these cells to PMDD immunisation. The model was then used to examine the effect of coadministration of the IL-10 gene. Its inclusion in the vaccine suppressed the response to antigen. This effect was maximal when the IL-10 gene was expressed in the same cell as the antigen gene. Using sequential immunisations the model was extended in order to study long-term effects, namely tolerance and the induction of regulatory T cells. Finally a mouse model of allergic asthma was used to examine any tolerogenic/therapeutic effects of the antigen-IL-10 vaccine. No significant longterm tolerance to antigen was identified. These results demonstrate that whilst the presence of IL-10 clearly inhibits the T cell response to antigen it does not necessarily confer tolerogenic properties on these cells. This brings into question whether IL-10 in the periphery, supplied, for example, by TR1 cells, generates fresh regulatory T cells or merely inhibits the response to a particular antigenic challenge.
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Horne, Phillip Howard. "Activation and effector function of unconventional acute rejection pathways studied in a hepatocellular allograft model." Columbus, Ohio : Ohio State University, 2007. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1188397900.

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Serr, Isabelle Daniela Verfasser], Anette-Gabriele [Akademischer Betreuer] Ziegler, de Angelis Martin [Gutachter] [Hrabé, Ludger [Gutachter] Klein, and Anette-Gabriele [Gutachter] Ziegler. "T cell activation versus tolerance induction in islet autoimmunity / Isabelle Daniela Serr ; Gutachter: Martin Hrabé de Angelis, Ludger Klein, Anette-Gabriele Ziegler ; Betreuer: Anette-Gabriele Ziegler." München : Universitätsbibliothek der TU München, 2018. http://d-nb.info/1168380286/34.

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Books on the topic "T cell activation/tolerance"

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Nicholaus, Zavazava, ed. T-cell, tolerance, transplantation, tumor. Lengerich: Pabst Science Publishers, 1995.

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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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Phillips, Roderick J. Biochemical mechanisms underlying T-cell activation. Uxbridge: Brunel University, 1990.

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A, Koretzky Gary, ed. T cell activation I: Proximal events. Copenhagen: Blackwell Munksgaard, 2003.

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Perkins, Philip. T cell activation in rheumatoid arthritis. Birmingham: University of Birmingham, 1995.

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Yuan, Dennis Jinglun. Mechanical regulation of T cell activation. [New York, N.Y.?]: [publisher not identified], 2021.

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A, Koretzky Gary, ed. T cell activation II: Signal integration. Copenhagen: Blackwell Munksgaard, 2003.

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Azuma, Miyuki, and Hideo Yagita, eds. Co-signal Molecules in T Cell Activation. Singapore: Springer Singapore, 2019. http://dx.doi.org/10.1007/978-981-32-9717-3.

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Moody, D. Branch, ed. T Cell Activation by CD1 and Lipid Antigens. Berlin, Heidelberg: Springer Berlin Heidelberg, 2007. http://dx.doi.org/10.1007/978-3-540-69511-0.

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Chen, Haoqian. Spatial Organization of CD28 Modulates T-cell Activation. [New York, N.Y.?]: [publisher not identified], 2016.

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Book chapters on the topic "T cell activation/tolerance"

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Holler, Ernst, Hildegard Greinix, and Robert Zeiser. "Acute Graft-Versus-Host Disease." In The EBMT Handbook, 385–93. Cham: Springer International Publishing, 2024. http://dx.doi.org/10.1007/978-3-031-44080-9_43.

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AbstractAcute graft-versus-host disease (GvHD) remains a major course of short term (100 days and 1 yr) mortality and morbidity after allogeneic stem cell transplantation. The pathophysiology of GvHD is described as a 3 step process starting with initial tissue damage by conditioning followed by host antigen presenting cell activation by damage and pathogen associated molecular patterns and finally resulting in activation of alloreactive T cells and proinflmmatory cytokines inducing target cell apoptosis. This activating cycle elicits multiple regulatory mechanisms and cells such as regulatory T cells and myeloid derived suppressor cells. Besides the disturbed balance between immune activation and immune tolerance, a disturbed capacity of tissue repair contributes to clincal damage.
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Blackman, Marcia A., John W. Kappler, and Philippa Marrack. "Multiple Mechanisms of T Cell Tolerance to Mls-la." In Mechanisms of Lymphocyte Activation and Immune Regulation III, 159–65. Boston, MA: Springer US, 1991. http://dx.doi.org/10.1007/978-1-4684-5943-2_18.

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Greco, Raffaella, and Dominique Farge. "CART Cells and Other Cell Therapies (ie MSC, Tregs) in Autoimmune Diseases." In The EBMT Handbook, 837–48. Cham: Springer International Publishing, 2024. http://dx.doi.org/10.1007/978-3-031-44080-9_93.

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AbstractAuto-immune diseases (AD) are heterogeneous conditions, characterized by polyclonal activation of the immune system with a defect of B or T lymphocyte selection and altered lymphocytic reactions to auto-antigens components (Burnet 1959a, b), although it is rare to identify a single antigenic epitope. The native immune system and its tissue environment play an important role to determine if exposure to a given antigen will induce an immune response or tolerance or anergy. The role of the genes coding for the major histocompatibility system molecules, but also of many other genes, is important in the regulation of the immune response, although this does not explain all the observed phenomena during loss of tolerance (Matzinger 1994; Rioux and Abbas 2005).
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Antunes, Mário J., and Manuel E. Correia. "Self Tolerance by Tuning T-Cell Activation: An Artificial Immune System for Anomaly Detection." In Lecture Notes of the Institute for Computer Sciences, Social Informatics and Telecommunications Engineering, 1–15. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-32615-8_1.

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Alexander, Tobias, Basil Sharrack, Montserrat Rovira, Riccardo Saccardi, Dominique Farge, John A. Snowden, and Raffaella Greco. "Autoimmune Disease." In The EBMT Handbook, 825–36. Cham: Springer International Publishing, 2024. http://dx.doi.org/10.1007/978-3-031-44080-9_92.

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AbstractAutoimmune diseases (ADs) are a heterogeneous group of diseases affecting 8–10% of the Western population, which constitute a heavy burden to society and are often debilitating and disabling for affected individuals. ADs are defined as an impairment of the immune system resulting in the loss of immune tolerance against self-tissues, by the existence of autoreactive T and B cells and by a complex mechanism of multifactorial aetiology, across genetics and environmental factors (Alexander and Greco 2022). Autoimmunity is also linked to autoinflammation, having common features as the activation against self, with subsequent systemic inflammation (Chap. 93).
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Ranganathan, Shoba. "T Cell Activation." In Encyclopedia of Systems Biology, 2115. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4419-9863-7_912.

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Charpentier, Bernard, Pascale Alard, Christian Hiesse, and Olivier Lantz. "Peripheral T Cell Tolerance." In Rejection and Tolerance, 217–25. Dordrecht: Springer Netherlands, 1994. http://dx.doi.org/10.1007/978-94-011-0802-7_22.

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Miller, J. F. A. P., W. R. Heath, J. Allison, G. Morahan, M. Hoffmann, C. Kurts, and H. Kosaka. "T Cell Tolerance and Autoimmunity." In Ciba Foundation Symposium 204 - The Molecular Basis of Cellular Defence Mechanisms, 159–71. Chichester, UK: John Wiley & Sons, Ltd., 2007. http://dx.doi.org/10.1002/9780470515280.ch11.

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Wagner, Hermann, and Klaus Heeg. "Mechanisms of T-Cell Activation." In Lymphohaematopoietic Growth Factors in Cancer Therapy, 19–23. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-76037-2_3.

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Solinger, A. M. "T-cell activation and function." In Immunopathogenetic Mechanisms of Arthritis, 86–100. Dordrecht: Springer Netherlands, 1988. http://dx.doi.org/10.1007/978-94-009-1293-9_5.

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Conference papers on the topic "T cell activation/tolerance"

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Eun, So-Young. "Abstract 1645: CEACAM1-blockade for T-cell activation and antitumor T-cell response." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-1645.

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Toussaint, Nora C., Magdalena Feldhahn, Matthias Ziehm, Stefan Stevanović, and Oliver Kohlbacher. "T-cell epitope prediction based on self-tolerance." In the 2nd ACM Conference. New York, New York, USA: ACM Press, 2011. http://dx.doi.org/10.1145/2147805.2147905.

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Thomas, R. "SP0130 Towards t cell tolerance in rheumatoid arthritis." In Annual European Congress of Rheumatology, EULAR 2018, Amsterdam, 13–16 June 2018. BMJ Publishing Group Ltd and European League Against Rheumatism, 2018. http://dx.doi.org/10.1136/annrheumdis-2018-eular.7793.

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Sheng, Michael, Catherine Le, Cordelia Dunai, Lam Khuat, Logan Vick, Kevin Stoffel, Arta Monjazeb, Craig Collins, Robert Canter, and William Murphy. "520 PD-1 Inhibits Bystander T Cell Activation and Protects from Activation Induced Cell Death." In SITC 37th Annual Meeting (SITC 2022) Abstracts. BMJ Publishing Group Ltd, 2022. http://dx.doi.org/10.1136/jitc-2022-sitc2022.0520.

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Weiss, Vivian L., Timothy H. Lee, Todd D. Armstrong, and Elizabeth M. Jaffee. "Abstract 1923: Regulatory T-cell subsets suppress high avidity CD8 T-cell activation and trafficking." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-1923.

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Skala, Melissa C., Alex J. Walsh, Kelsey Tweed, Katie Mueller, Isabel Jones, Steven M. Trier, and Krishanu Saha. "Label-free classification of T cell activation (Conference Presentation)." In Multiphoton Microscopy in the Biomedical Sciences XX, edited by Ammasi Periasamy, Peter T. So, and Karsten König. SPIE, 2020. http://dx.doi.org/10.1117/12.2546366.

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Lajoie, Marc J., Gabriel Butterfield, Elizabeth Gray, Kate DaPron, Daniel Stetson, David Baker, and Neil King. "Abstract B073: Protein nanoparticles for controllable T cell activation." In Abstracts: Second CRI-CIMT-EATI-AACR International Cancer Immunotherapy Conference: Translating Science into Survival; September 25-28, 2016; New York, NY. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/2326-6066.imm2016-b073.

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Tanimoto, Kazushi, Sawa Ito, Samantha Miner, Pawel Muranski, Nancy F. Hensel, J. Joseph Melenhorst, and A. John Barrett. "Abstract 1272: Myeloid leukemia cell lines suppress T cell activation and proliferation." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-1272.

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Stecha, Pete, Denise Garvin, Jim Hartnett, Brad Swanson, Frank Fan, Mei Cong, and Zhi-jie Jey Cheng. "Abstract 1215: Improved T cell activation bioassays for development of bispecific antibodies and engineered T cell immunotherapies." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-1215.

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Stecha, Pete, Denise Garvin, Jim Hartnett, Brad Swanson, Frank Fan, Mei Cong, and Zhi-jie Jey Cheng. "Abstract 1215: Improved T cell activation bioassays for development of bispecific antibodies and engineered T cell immunotherapies." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-1215.

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Reports on the topic "T cell activation/tolerance"

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Cook-Mills, Joan M., Hidayatulla G. Munshi, Robert L. Perlman, and Donald A. Chambers. Mouse Hepatitis Virus Infection Suppresses Modulation of Mouse Spleen T- Cell Activation. Fort Belvoir, VA: Defense Technical Information Center, January 1988. http://dx.doi.org/10.21236/ada237464.

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Ladle, Brian H., and Elizabeth M. Jaffee. Dissecting the Mechanism of T Cell Tolerance for More Effective Breast Cancer Vaccine Development. Fort Belvoir, VA: Defense Technical Information Center, August 2004. http://dx.doi.org/10.21236/ada435335.

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Nelson, Brad H. Eliciting Autoimmunity to Ovarian Tumors in Mice by Genetic Disruption of T Cell Tolerance Mechanisms. Fort Belvoir, VA: Defense Technical Information Center, August 2002. http://dx.doi.org/10.21236/ada409619.

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Nelson, Brad H. Eliciting Autoimmunity to Ovarian Tumors in Mice by Genetic Disruption of T Cell Tolerance Mechanisms. Fort Belvoir, VA: Defense Technical Information Center, August 2006. http://dx.doi.org/10.21236/ada462679.

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Hurwitz, Arthur A. Modulation of T Cell Tolerance in a Murine Model for Immunotherapy of Prostatic Adenocarcinoma. Addendum. Fort Belvoir, VA: Defense Technical Information Center, September 2007. http://dx.doi.org/10.21236/ada475839.

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Kwon, Eugene D. Lowering T Cell Activation Thresholds and Deregulating Homeostasis to Facilitate Immunotherapeutic Responses to Treat Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, April 2005. http://dx.doi.org/10.21236/ada460762.

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Kwon, Eugene D. Lowering T Cell Activation Thresholds and Deregulating Homeostasis to Facilitate Immunotherapeutic Responses to Treat Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, June 2006. http://dx.doi.org/10.21236/ada460766.

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Powell, Jonathan. Selective Inhibition of T Cell Tolerance as a Means of Enhancing Tumor Vaccines in a Mouse Model of Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, June 2006. http://dx.doi.org/10.21236/ada460797.

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Fromm, A., Avihai Danon, and Jian-Kang Zhu. Genes Controlling Calcium-Enhanced Tolerance to Salinity in Plants. United States Department of Agriculture, March 2003. http://dx.doi.org/10.32747/2003.7585201.bard.

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The specific objectives of the proposed research were to identify, clone and characterize downstream cellular target(s) of SOS3 in Arabidopsis thaliana, to analyze the Ca2+-binding characteristics of SOS3 and the sos3-1 mutant and their interactions with SOS3 cellular targets to analyze the SOS3 cell-specific expression patterns, and its subcellular localization, and to assess the in vivo role of SOS3 target protein(s) in plant tolerance to salinity stress. In the course of the study, in view of recent opportunities in identifying Ca2+ - responsive genes using microarrays, the group at Weizmann has moved into identifying Ca2+-responsive stress genes by using a combination of aqeuorin-based measurements of cytosolic Ca and analysis by DNA microarrays of early Ca-responsive genes at the whole genome level. Analysis of SOS3 (University of Arizona) revealed its expression in both roots and shoots. However, the expression of this gene is not induced by stress. This is reminiscent of other stress proteins that are regulated by post-transcriptional mechanisms such as the activation by second messengers like Ca. Further analysis of the expression of the gene using promoter - GUS fusions revealed expression in lateral root primordial. Studies at the Weizmann Institute identified a large number of genes whose expression is up-regulated by a specific cytosolic Ca burst evoked by CaM antagonists. Fewer genes were found to be down-regulated by the Ca burst. Among the up-regulated genes many are associated with early stress responses. Moreover, this study revealed a large number of newly identified Ca-responsive genes. These genes could be useful to investigate yet unknown Ca-responsive gene networks involved in plant response to stress.
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Locy, Robert D., Hillel Fromm, Joe H. Cherry, and Narendra K. Singh. Regulation of Arabidopsis Glutamate Decarboxylase in Response to Heat Stress: Modulation of Enzyme Activity and Gene Expression. United States Department of Agriculture, January 2001. http://dx.doi.org/10.32747/2001.7575288.bard.

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Most plants accumulate the nonprotein amino acid, g-aminobutyric acid (GABA), in response to heat stress. GABA is made from glutamate in a reaction catalyzed by glutamate decarboxylase (GAD), an enzyme that has been shown by the Israeli PI to be a calmodulin (CaM) binding protein whose activity is regulated in vitro by calcium and CaM. In Arabidopsis there are at least 5 GAD genes, two isoforms of GAD, GAD1 and GAD2, are known to be expressed, both of which appear to be calmodulin-binding proteins. The role of GABA accumulation in stress tolerance remains unclear, and thus the objectives of the proposed work are intended to clarify the possible roles of GABA in stress tolerance by studying the factors which regulate the activity of GAD in vivo. Our intent was to demonstrate the factors that mediate the expression of GAD activity by analyzing the promoters of the GAD1 and GAD2 genes, to determine the role of stress induced calcium signaling in the regulation of GAD activity, to investigate the role of phosphorylation of the CaM-binding domain in the regulation of GAD activity, and to investigate whether ABA signaling could be involved in GAD regulation via the following set of original Project Objectives: 1. Construction of chimeric GAD1 and GAD2 promoter/reporter gene fusions and their utilization for determining cell-specific expression of GAD genes in Arabidopsis. 2. Utilizing transgenic plants harboring chimeric GAD1 promoter-luciferase constructs for isolating mutants in genes controlling GAD1 gene activation in response to heat shock. 3. Assess the role of Ca2+/CaM in the regulation of GAD activity in vivo in Arabidopsis. 4. Study the possible phosphorylation of GAD as a means of regulation of GAD activity. 5. Utilize ABA mutants of Arabidopsis to assess the involvement of this phytohormone in GAD activation by stress stimuli. The major conclusions of Objective 1 was that GAD1 was strongly expressed in the elongating region of the root, while GAD2 was mainly expressed along the phloem in both roots and shoots. In addition, GAD activity was found not to be transcriptionally regulated in response to heat stress. Subsequently, The Israeli side obtained a GAD1 knockout mutation, and in light of the objective 1 results it was determined that characterization of this knockout mutation would contribute more to the project than the proposed Objective 2. The major conclusion of Objective 3 is that heat-stress-induced changes in GAD activity can be explained by heat-stress-induced changes in cytosolic calcium levels. No evidence that GAD activity was transcriptionally or translationally regulated or that protein phosphorylation was involved in GAD regulation (objective 4) was obtained. Previously published data by others showing that in wheat roots ABA regulated GABA accumulation proved not to be the case in Arabidopsis (Objective 5). Consequently, we put the remaining effort in the project into the selection of mutants related to temperature adaptation and GABA utilization and attempting to characterize events resulting from GABA accumulation. A set of 3 heat sensitive mutants that appear to have GABA related mutations have been isolated and partially characterized, and a study linking GABA accumulation to growth stimulation and altered nitrate assimilation were conducted. By providing a better understanding of how GAD activity was and was not regulated in vivo, we have ruled out the use of certain genes for genetically engineering thermotolerance, and suggested other areas of endeavor related to the thrust of the project that may be more likely approaches to genetically engineering thermotolerance.
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