Journal articles: 'Peripheral t cell tolerance'

1

Miller, Jacques F. A. P., and Grant Morahan. "Peripheral T Cell Tolerance." Annual Review of Immunology 10, no. 1 (April 1992): 51–69. http://dx.doi.org/10.1146/annurev.iy.10.040192.000411.

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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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Arnold, Bernd. "Levels of peripheral T cell tolerance." Transplant Immunology 10, no. 2-3 (August 2002): 109–14. http://dx.doi.org/10.1016/s0966-3274(02)00056-4.

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Xing, Y., and K. A. Hogquist. "T-Cell Tolerance: Central and Peripheral." Cold Spring Harbor Perspectives in Biology 4, no. 6 (June 1, 2012): a006957. http://dx.doi.org/10.1101/cshperspect.a006957.

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Lechler, R., and F. M. Marelli-Berg. "Mechanisms of peripheral T-cell tolerance." Journal of Viral Hepatitis 4, s2 (November 1997): 1–5. http://dx.doi.org/10.1111/j.1365-2893.1997.tb00174.x.

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de St. Groth, Barbara Fazekas. "DCs and peripheral T cell tolerance." Seminars in Immunology 13, no. 5 (October 2001): 311–21. http://dx.doi.org/10.1006/smim.2001.0327.

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Lutz, Manfred B., and Christian Kurts. "Induction of peripheral CD4+ T-cell tolerance and CD8+ T-cell cross-tolerance by dendritic cells." European Journal of Immunology 39, no. 9 (August 21, 2009): 2325–30. http://dx.doi.org/10.1002/eji.200939548.

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Lechler, Robert, Jian-Guo Chai, Federica Marelli-Berg, and Giovanna Lombardi. "The contributions of T-cell anergy to peripheral T-cell tolerance." Immunology 103, no. 3 (July 2001): 262–69. http://dx.doi.org/10.1046/j.1365-2567.2001.01250.x.

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Wells, Andrew D., Xian–Chang Li, Terry B. Strom, and Laurence A. Turka. "The role of peripheral T–cell deletion in transplantation tolerance." Philosophical Transactions of the Royal Society of London. Series B: Biological Sciences 356, no. 1409 (May 29, 2001): 617–23. http://dx.doi.org/10.1098/rstb.2001.0845.

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The apoptotic deletion of thymocytes that express self–reactive antigen receptors is the basis of central (thymic) self–tolerance. However, it is clear that some autoreactive T cells escape deletion in the thymus and exist as mature lymphocytes in the periphery. Therefore, peripheral mechanisms of tolerance are also crucial, and failure of these peripheral mechanisms leads to autoimmunity. Clonal deletion, clonal anergy and immunoregulation and/or suppression have been suggested as mechanisms by which ‘inappropriate’ T–lymphocyte responses may be controlled in the periphery. Peripheral clonal deletion, which involves the apoptotic elimination of lymphocytes, is critical for T–cell homeostasis during normal immune responses, and is recognized as an important process by which self–tolerance is maintained. Transplantation of foreign tissue into an adult host represents a special case of ‘inappropriate’ T–cell reactivity that is subject to the same central and peripheral tolerance mechanisms that control reactivity against self. In this case, the unusually high frequency of naive T cells able to recognize and respond against non–self–allogeneic major histocompatibility complex (MHC) antigens leads to an exceptionally large pool of pathogenic effector lymphocytes that must be controlled if graft rejection is to be avoided. A great deal of effort has been directed toward understanding the role of clonal anergy and/or active immunoregulation in the induction of peripheral transplantation tolerance but, until recently, relatively little progress had been made towards defining the potential contribution of clonal deletion. Here, we outline recent data that define a clear requirement for deletion in the induction of peripheral transplantation tolerance across MHC barriers, and discuss the potential implications of these results in the context of current treatment modalities used in the clinical transplantation setting.

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Hickman, Somia P., and Laurence A. Turka. "Homeostatic T cell proliferation as a barrier to T cell tolerance." Philosophical Transactions of the Royal Society B: Biological Sciences 360, no. 1461 (August 16, 2005): 1713–21. http://dx.doi.org/10.1098/rstb.2005.1699.

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The maintenance of T cell numbers in the periphery is mediated by distinct homeostatic mechanisms that ensure the proper representation of naïve and memory T cells. Homeostatic proliferation refers to the process by which T cells in lymphopenic hosts divide in the absence of cognate antigen to reconstitute the peripheral lymphoid compartment. During this process T cells acquire effector-memory like properties, including the ability to respond to low doses of antigen in the absence of CD28 costimulation. Furthermore, this capacity is retained long after proliferation has ceased. Accumulating data implicates homeostatic proliferation in autoimmune diseases and transplant rejection, and suggests that it may represent a barrier to tolerance in protocols that use T cell depletion. Implementing combination therapies that aim to promote the development and expansion of regulatory T cell populations while specifically targeting alloresponsive T cells may be the soundest approach to attaining allograft tolerance in the aftermath of T cell depletion and homeostatic proliferation.

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11

MILLER, JACQUES F. A. P. "A transgenic window on peripheral T cell tolerance." Immunology and Cell Biology 70, no. 1 (February 1992): 49–50. http://dx.doi.org/10.1038/icb.1992.7.

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12

Li, Dongbei, Haijun Li, Haiying Fu, Kunwei Niu, Yantong Guo, Chuan Guo, Jitong Sun, Yi Li, and Wei Yang. "Aire-Overexpressing Dendritic Cells Induce Peripheral CD4+ T Cell Tolerance." International Journal of Molecular Sciences 17, no. 1 (December 29, 2015): 38. http://dx.doi.org/10.3390/ijms17010038.

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13

Vella, A. T., M. T. Scherer, L. Schultz, J. W. Kappler, and P. Marrack. "B cells are not essential for peripheral T-cell tolerance." Proceedings of the National Academy of Sciences 93, no. 2 (January 23, 1996): 951–55. http://dx.doi.org/10.1073/pnas.93.2.951.

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14

Yamano, Tomoyoshi, Sho Watanabe, Hiroyuki Hasegawa, Toshihiro Suzuki, Ryo Abe, Hideaki Tahara, Takeshi Nitta, Naozumi Ishimaru, Jonathan Sprent, and Hidehiro Kishimoto. "Ex vivo–expanded DCs induce donor-specific central and peripheral tolerance and prolong the acceptance of donor skin grafts." Blood 117, no. 9 (March 3, 2011): 2640–48. http://dx.doi.org/10.1182/blood-2010-07-293860.

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Abstract Dendritic cells (DCs) are known to regulate immune responses by inducing both central and peripheral tolerance. DCs play a vital role in negative selection of developing thymocytes by deleting T cells with high-affinity for self-peptide–major histocompatibility complexes. In the periphery, DCs mediate peripheral tolerance by promoting regulatory T-cell development, induction of T-cell unresponsiveness, and deletion of activated T cells. We studied whether allogeneic DCs, obtained from bone marrow cultured with either Flt3L (FLDCs) or granulocyte-macrophage colony-stimulating factor (GMDCs), could induce allospecific central and peripheral tolerance after IV injection; B cells were used as a control. The results showed that only FLDCs reached the thymus after injection and that these cells induced both central and peripheral tolerance to donor major histocompatibility complexes. For central tolerance, injection of FLDCs induced antigen-specific clonal deletion of both CD8 and CD4 single-positive thymocytes. For peripheral tolerance, injection of FLDCs induced donor-specific T-cell unresponsiveness and prolonged survival of donor-derived skin grafts. Tolerance induction by adoptive transfer of FLDCs could be a useful approach for promoting graft acceptance after organ transplantation.

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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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Falb, Dean, Thomas J. Briner, Geoffrey H. Sunshine, Cheryl R. Bourque, Mohammad Luqman, Malcolm L. Gefter, and Thomas Kamradt. "Peripheral tolerance in T cell receptor-transgenic mice: Evidence for T cell anergy." European Journal of Immunology 26, no. 1 (January 1996): 130–35. http://dx.doi.org/10.1002/eji.1830260120.

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17

Srinivasan, Mathangi, and Kenneth A. Frauwirth. "Peripheral tolerance in CD8+ T cells." Cytokine 46, no. 2 (May 2009): 147–59. http://dx.doi.org/10.1016/j.cyto.2009.01.010.

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18

Tindle, Robert W. "Peripheral T-Cell Tolerance Defined through Transgenic Mouse Studies." Autoimmunity 33, no. 2 (January 2001): 135–49. http://dx.doi.org/10.3109/08916930108995998.

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19

Klann, Jane E., Stephanie H. Kim, Kelly A. Remedios, Zhaoren He, Patrick J. Metz, Justine Lopez, Tiffani Tysl, et al. "Integrin Activation Controls Regulatory T Cell–Mediated Peripheral Tolerance." Journal of Immunology 200, no. 12 (April 27, 2018): 4012–23. http://dx.doi.org/10.4049/jimmunol.1800112.

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20

Bansal-Pakala, Pratima, Amha Gebre-Hiwot Jember, and Michael Croft. "Signaling through OX40 (CD134) breaks peripheral T-cell tolerance." Nature Medicine 7, no. 8 (August 2001): 907–12. http://dx.doi.org/10.1038/90942.

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21

Forman, D., E. S. Kang, C. Tian, and J. Iacomini. "PERIPHERAL CD4 T CELL TOLERANCE INDUCED BY GENE THERAPY." Transplantation 78 (July 2004): 532. http://dx.doi.org/10.1097/00007890-200407271-01434.

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22

Zhao, Bingjie, Lu Chang, Haiying Fu, Guangyu Sun, and Wei Yang. "The Role of Autoimmune Regulator (AIRE) in Peripheral Tolerance." Journal of Immunology Research 2018 (September 4, 2018): 1–6. http://dx.doi.org/10.1155/2018/3930750.

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Autoimmune regulator (AIRE), whose gene mutation is considered to be a causative factor of autoimmune polyglandular syndrome type 1 (APS1), is an important transcriptional regulator. Studies on the role of AIRE in the central immune system have demonstrated that AIRE can eliminate autoreactive T cells by regulating the expression of a series of tissue specific antigens promiscuously in medullary thymic epithelial cells (mTECs) and induce regulatory T cell (Treg) production to maintain central immune tolerance. However, the related research of AIRE in peripheral tolerance is few. In order to understand the current research progress on AIRE in peripheral tolerance, this review mainly focuses on the expression and distribution of AIRE in peripheral tissues and organs, and the role of AIRE in peripheral immune tolerance such as regulating Toll-like receptor (TLR) expression and the maturation status of antigen presenting cells (APCs), inducing T cell tolerance and differentiation. This review will show us that AIRE also plays an indispensable role in the periphery.

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23

Wekerle, Thomas, Mohamed H. Sayegh, Joshua Hill, Yong Zhao, Anil Chandraker, Kirsten G. Swenson, Guiling Zhao, and Megan Sykes. "Extrathymic T Cell Deletion and Allogeneic Stem Cell Engraftment Induced with Costimulatory Blockade Is Followed by Central T Cell Tolerance." Journal of Experimental Medicine 187, no. 12 (June 15, 1998): 2037–44. http://dx.doi.org/10.1084/jem.187.12.2037.

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A reliable, nontoxic method of inducing transplantation tolerance is needed to overcome the problems of chronic organ graft rejection and immunosuppression-related toxicity. Treatment of mice with single injections of an anti-CD40 ligand antibody and CTLA4Ig, a low dose (3 Gy) of whole body irradiation, plus fully major histocompatibility complex–mismatched allogeneic bone marrow transplantation (BMT) reliably induced high levels (>40%) of stable (>8 mo) multilineage donor hematopoiesis. Chimeric mice permanently accepted donor skin grafts (>100 d), and rapidly rejected third party grafts. Progressive deletion of donor-reactive host T cells occurred among peripheral CD4+ lymphocytes, beginning as early as 1 wk after bone marrow transplantation. Early deletion of peripheral donor-reactive host CD4 cells also occurred in thymectomized, similarly treated marrow recipients, demonstrating a role for peripheral clonal deletion of donor-reactive T cells after allogeneic BMT in the presence of costimulatory blockade. Central intrathymic deletion of newly developing T cells ensued after donor stem cell engraftment had occurred. Thus, we have shown that high levels of chimerism and systemic T cell tolerance can be reliably achieved without myeloablation or T cell depletion of the host. Chronic immunosuppression and rejection are avoided with this powerful, nontoxic approach to inducing tolerance.

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24

Magrone, Thea, and Emilio Jirillo. "The Tolerant Immune System: Biological Significance and Clinical Implications of T Cell Tolerance." Endocrine, Metabolic & Immune Disorders - Drug Targets 19, no. 5 (June 3, 2019): 580–93. http://dx.doi.org/10.2174/1871530319666181211161721.

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Background: T cell tolerance both at thymic and peripheral levels is a mechanism of protection finalized to eradicate autoreactive T cell clones and/or to maintain immune homeostasis, especially, postnatally. Central tolerance occurs in the thymic medulla via a mechanism of negative selection which leads to the eradication of autoreactive T cell clones. Mechanisms of Action: Such a tolerogenic event relies on Fas-mediated apoptosis of autoreactive T cell clones operated by thymic dendritic cells (DCs), on the one hand. On the other hand, activated thymic T regulatory (Treg) cells in cooperation with medullary thymic epithelial cells and DCs suppress autoreactive T cell clones. Peripherally, different types of Treg cells exert the so-called peripheral tolerance towards autoreactive T cell clones which may have escaped from negative selection mechanisms. At the same time, peripheral Treg cells activated by tolerogenic DC have antiinflammatory activities, especially in the intestine towards food and microbial antigens. Drug Targeting: Various natural and dietary products, such as vitamins (A, C, D), lactobacilli and polyphenols will be described for their tolerogenic capacity to attenuate the inflammatory pathway, as observed in preclinical and clinical studies.

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Mirshahidi, Saied, Ching-Tai Huang, and Scheherazade Sadegh-Nasseri. "Anergy in Peripheral Memory Cd4+ T Cells Induced by Low Avidity Engagement of T Cell Receptor." Journal of Experimental Medicine 194, no. 6 (September 10, 2001): 719–32. http://dx.doi.org/10.1084/jem.194.6.719.

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Induction of tolerance in self-reactive memory T cells is an important process in the prevention of autoimmune responses against peripheral self-antigens in autoimmune diseases. Although naive T cells can readily be tolerized, memory T cells are less susceptible to tolerance induction. Recently, we demonstrated that low avidity engagement of T cell receptor (TCR) by low densities of agonist peptides induced anergy in T cell clones. Since memory T cells are more responsive to lower antigenic stimulation, we hypothesized that a low avidity TCR engagement may induce tolerance in memory T cells. We have explored two antigenic systems in two transgenic mouse models, and have tracked specific T cells that are primed and show memory phenotype. We demonstrate that memory CD4+ T cells can be rendered anergic by presentation of low densities of agonist peptide–major histocompatibility complex complexes in vivo. We rule out other commonly accepted mechanisms for induction of T cell tolerance in vivo, such as deletion, ignorance, or immunosuppression. Anergy is the most likely mechanism because addition of interleukin 2–reversed anergy in specific T cells. Moreover, cytotoxic T lymphocyte antigen (CTLA)-4 plays a critical role in the induction of anergy because we observed that there was increased surface expression of CTLA-4 on anergized T cells, and that injection of anti–CTLA-4 blocking antibody restored anergy in vivo.

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26

Miller, Jacques F. A. P., and Richard A. Flavell. "T-cell tolerance and autoimmunity in transgenic models of central and peripheral tolerance." Current Opinion in Immunology 6, no. 6 (December 1994): 892–99. http://dx.doi.org/10.1016/0952-7915(94)90010-8.

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27

Lucas, Carrie L., Creg J. Workman, Semir Beyaz, Samuel LoCascio, Guiling Zhao, Dario A. A. Vignali, and Megan Sykes. "LAG-3, TGF-β, and cell-intrinsic PD-1 inhibitory pathways contribute to CD8 but not CD4 T-cell tolerance induced by allogeneic BMT with anti-CD40L." Blood 117, no. 20 (May 19, 2011): 5532–40. http://dx.doi.org/10.1182/blood-2010-11-318675.

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Abstract Administration of a single dose of anti-CD40L mAb at the time of allogeneic BM transplantation tolerizes peripheral alloreactive T cells and permits establishment of mixed hematopoietic chimerism in mice. Once engrafted, mixed chimeras are systemically tolerant to donor Ags through a central deletion mechanism and will accept any donor organ indefinitely. We previously found that the PD-1/PD-L1 pathway is required for CD8 T-cell tolerance in this model. However, the cell population that must express PD-1 and the role of other inhibitory molecules were unknown. Here, we report that LAG-3 is required for long-term peripheral CD8 but not CD4 T-cell tolerance and that this requirement is CD8 cell-extrinsic. In contrast, adoptive transfer studies revealed a CD8 T cell–intrinsic requirement for CTLA4/B7.1/B7.2 and for PD-1 for CD8 T-cell tolerance induction. We also observed that both PD-L1 and PD-L2 are independently required on donor cells to achieve T-cell tolerance. Finally, we uncovered a requirement for TGF-β signaling into T cells to achieve peripheral CD8 but not CD4 T-cell tolerance in this in vivo system.

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Chen, Xiufen, Douglas E. Kline, and Justin Kline. "Peripheral T-cell tolerance in hosts with acute myeloid leukemia." OncoImmunology 2, no. 8 (August 2013): e25445. http://dx.doi.org/10.4161/onci.25445.

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29

Anderson, Colin, C. "Mechanisms and models of peripheral CD4 T cell self-tolerance." Frontiers in Bioscience 9, no. 1-3 (2004): 2947. http://dx.doi.org/10.2741/1450.

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30

Kreuwel, Huub T. C., Judith A. Biggs, Ingrid M. Pilip, Eric G. Pamer, David Lo, and Linda A. Sherman. "Defective CD8+ T Cell Peripheral Tolerance in Nonobese Diabetic Mice." Journal of Immunology 167, no. 2 (July 15, 2001): 1112–17. http://dx.doi.org/10.4049/jimmunol.167.2.1112.

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31

Keir, Mary E., Spencer C. Liang, Indira Guleria, Yvette E. Latchman, Andi Qipo, Lee A. Albacker, Maria Koulmanda, Gordon J. Freeman, Mohamed H. Sayegh, and Arlene H. Sharpe. "Tissue expression of PD-L1 mediates peripheral T cell tolerance." Journal of Experimental Medicine 203, no. 4 (April 10, 2006): 883–95. http://dx.doi.org/10.1084/jem.20051776.

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Programmed death 1 (PD-1), an inhibitory receptor expressed on activated lymphocytes, regulates tolerance and autoimmunity. PD-1 has two ligands: PD-1 ligand 1 (PD-L1), which is expressed broadly on hematopoietic and parenchymal cells, including pancreatic islet cells; and PD-L2, which is restricted to macrophages and dendritic cells. To investigate whether PD-L1 and PD-L2 have synergistic or unique roles in regulating T cell activation and tolerance, we generated mice lacking PD-L1 and PD-L2 (PD-L1/PD-L2−/− mice) and compared them to mice lacking either PD-L. PD-L1 and PD-L2 have overlapping functions in inhibiting interleukin-2 and interferon-γ production during T cell activation. However, PD-L1 has a unique and critical role in controlling self-reactive T cells in the pancreas. Our studies with bone marrow chimeras demonstrate that PD-L1/PD-L2 expression only on antigen-presenting cells is insufficient to prevent the early onset diabetes that develops in PD-L1/PD-L2−/− non-obese diabetic mice. PD-L1 expression in islets protects against immunopathology after transplantation of syngeneic islets into diabetic recipients. PD-L1 inhibits pathogenic self-reactive CD4+ T cell–mediated tissue destruction and effector cytokine production. These data provide evidence that PD-L1 expression on parenchymal cells rather than hematopoietic cells protects against autoimmune diabetes and point to a novel role for PD-1–PD-L1 interactions in mediating tissue tolerance.

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32

Weigle, William O., and Carole G. Romball. "CD4+ T-cell subsets and cytokines involved in peripheral tolerance." Immunology Today 18, no. 11 (November 1997): 533–38. http://dx.doi.org/10.1016/s0167-5699(97)01151-1.

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33

Serfling, Edgar, Stefan Klein-Hessling, Alois Palmetshofer, Tobias Bopp, Michael Stassen, and Edgar Schmitt. "NFAT transcription factors in control of peripheral T cell tolerance." European Journal of Immunology 36, no. 11 (November 2006): 2837–43. http://dx.doi.org/10.1002/eji.200536618.

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34

Buer, Jan, Astrid M. Westendorf, An-Ping Zeng, Feng He, Wiebke Hansen, and Michael Probst-Kepper. "Mechanisms of Central and Peripheral T-Cell Tolerance: An Update." Transfusion Medicine and Hemotherapy 32, no. 6 (2005): 384–99. http://dx.doi.org/10.1159/000089128.

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35

Kreuwel, Huub T. C., Sandra Aung, Cheryl Silao, and Linda A. Sherman. "Memory CD8+ T Cells Undergo Peripheral Tolerance." Immunity 17, no. 1 (July 2002): 73–81. http://dx.doi.org/10.1016/s1074-7613(02)00337-0.

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von Bubnoff, Dagmar, Daniel Hanau, Joerg Wenzel, Osamu Takikawa, Brian Hall, Susanne Koch, and Thomas Bieber. "Indoleamine 2,3-dioxygenase–expressing antigen-presenting cells and peripheral T-cell tolerance." Journal of Allergy and Clinical Immunology 112, no. 5 (November 2003): 854–60. http://dx.doi.org/10.1016/s0091-6749(03)02014-1.

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37

Broggi, Achille, Ivan Zanoni, and Francesca Granucci. "Migratory conventional dendritic cells in the induction of peripheral T cell tolerance." Journal of Leukocyte Biology 94, no. 5 (November 2013): 903–11. http://dx.doi.org/10.1189/jlb.0413222.

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38

Gurung, Prajwal, Tamara A. Kucaba, Stephen P. Schoenberger, Thomas A. Ferguson, and Thomas S. Griffith. "TRAIL-expressing CD8+ T cells mediate tolerance following soluble peptide-induced peripheral T cell deletion." Journal of Leukocyte Biology 88, no. 6 (August 31, 2010): 1217–25. http://dx.doi.org/10.1189/jlb.0610343.

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39

Parish, Ian A., Sudha Rao, Gordon K. Smyth, Torsten Juelich, Gareth S. Denyer, Gayle M. Davey, Andreas Strasser, and William R. Heath. "The molecular signature of CD8+ T cells undergoing deletional tolerance." Blood 113, no. 19 (May 7, 2009): 4575–85. http://dx.doi.org/10.1182/blood-2008-10-185223.

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Abstract Peripheral tolerance induction is critical for the maintenance of self-tolerance and can be mediated by immunoregulatory T cells or by direct induction of T-cell anergy or deletion. Although the molecular processes underlying anergy have been extensively studied, little is known about the molecular basis for peripheral T-cell deletion. Here, we determined the gene expression signature of peripheral CD8+ T cells undergoing deletional tolerance, relative to those undergoing immunogenic priming or lymphopenia-induced proliferation. From these data, we report the first detailed molecular signature of cells undergoing deletion. Consistent with defective cytolysis, these cells exhibited deficiencies in granzyme up-regulation. Furthermore, they showed antigen-driven Bcl-2 down-regulation and early up-regulation of the proapoptotic protein Bim, consistent with the requirement of this BH3-only protein for peripheral T-cell deletion. Bim up-regulation was paralleled by defective interleukin-7 receptor α (IL-7Rα) chain reexpression, suggesting that Bim-dependent death may be triggered by loss of IL-7/IL-7R signaling. Finally, we observed parallels in molecular signatures between deletion and anergy, suggesting that these tolerance pathways may not be as molecularly distinct as previously surmised.

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40

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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41

Rocha, B., A. Grandien, and A. A. Freitas. "Anergy and exhaustion are independent mechanisms of peripheral T cell tolerance." Journal of Experimental Medicine 181, no. 3 (March 1, 1995): 993–1003. http://dx.doi.org/10.1084/jem.181.3.993.

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We studied the interactions of male-specific T cell receptor (TCR)-alpha/beta-transgenic (TG) cells with different concentrations of male antigen in vivo. We constructed mouse chimeras expressing different amounts of male antigen by injecting thymectomized, lethally irradiated mice with various ratios of male (immunoglobulin [Ig] Ha) and female (IgHb) bone marrow. These chimeras were injected with male-specific TCR-alpha/beta-trangenic cells. These experiments allowed us to monitor antigen persistence and characterize antigen-specific T cells in terms of their frequency, reactivity, and effector functions (as tested by elimination of male B cells in vivo). In the absence of antigen, virgin TG cells persisted but did not expand. Transient exposure to antigen resulted in cell expansion, followed by the persistence of increased numbers of antigen-reactive T cells. In contrast, antigen persistence was followed by two independent mechanisms of tolerance induction: anergy (at high antigen concentrations), where T cells did not differentiate into effector functions but persisted in vivo as unresponsive T cells, and exhaustion (at lower antigen concentrations), where differentiation into effector functions (B cell elimination) occurred but was followed by the disappearance of antigen-specific T cells.

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42

Teague, Ryan M., Philip D. Greenberg, Carla Fowler, Maria Z. Huang, Xiaoxia Tan, Junko Morimoto, Michelle L. Dossett, Eric S. Huseby, and Claes Öhlén. "Peripheral CD8+ T Cell Tolerance to Self-Proteins Is Regulated Proximally at the T Cell Receptor." Immunity 28, no. 5 (May 2008): 662–74. http://dx.doi.org/10.1016/j.immuni.2008.03.012.

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43

Legge, Kevin L., Randal K. Gregg, Roberto Maldonado-Lopez, Lequn Li, Jacque C. Caprio, Muriel Moser, and Habib Zaghouani. "On the Role of Dendritic Cells in Peripheral T Cell Tolerance and Modulation of Autoimmunity." Journal of Experimental Medicine 196, no. 2 (July 15, 2002): 217–27. http://dx.doi.org/10.1084/jem.20011061.

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Recently, it has become clear that dendritic cells (DCs) are essential for the priming of T cell responses. However, their role in the maintenance of peripheral T cell tolerance remains largely undefined. Herein, an antigen-presenting cell (APC) transfer system was devised and applied to experimental allergic encephalomyelitis (EAE), to evaluate the contribution that DCs play in peripheral T cell tolerance. The CD8α−CD4+ subset, a minor population among splenic DCs, was found to mediate both tolerance and bystander suppression against diverse T cell specificities. Aggregated (agg) Ig-myelin oligodendrocyte glycoprotein (MOG), an Ig chimera carrying the MOG 35–55 peptide, binds and cross-links FcγR on APC leading to efficient peptide presentation and interleukin (IL)-10 production. Furthermore, administration of agg Ig-MOG into diseased mice induces relief from clinical EAE involving multiple epitopes. Such recovery could not occur in FcγR-deficient mice where both uptake of Ig-MOG and IL-10 production are compromised. However, reconstitution of these mice with DC populations incorporating the CD8α−CD4+ subset restored Ig-MOG–mediated reversal of EAE. Transfer of CD8α+ or even CD8α−CD4− DCs had no effect on the disease. These findings strongly implicate DCs in peripheral tolerance and emphasize their functional potency, as a small population of DCs was able to support effective suppression of autoimmunity.

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Paroli, Marino,. "Mechanisms of CD8+ T cell peripheral tolerance to our own antigens." Frontiers in Bioscience 10, no. 1-3 (2005): 1628. http://dx.doi.org/10.2741/1646.

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Cooper, Cristine J., and Pamela J. Fink. "Antigen Receptor Revision as a Mechanism of Peripheral T Cell Tolerance." Graft 5, no. 7 (October 2002): 383–89. http://dx.doi.org/10.1177/152216202237625.

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Charbonnier, Louis-Marie, Sen Wang, Peter Georgiev, Esen Sefik, and Talal A. Chatila. "Control of peripheral tolerance by regulatory T cell–intrinsic Notch signaling." Nature Immunology 16, no. 11 (October 5, 2015): 1162–73. http://dx.doi.org/10.1038/ni.3288.

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Maekawa, Yoichi, Shin-ichi Tsukumo, Hiroko Okada, Kenji Kishihara, and Koji Yasutomo. "Breakdown of peripheral T-cell tolerance by chronic interleukin-15 elevation1." Transplantation 76, no. 2 (July 2003): 415–20. http://dx.doi.org/10.1097/01.tp.0000078900.71840.2b.

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Miller, J. F. A. P., G. Morahan, J. Allison, and M. Hoffmann. "A Transgenic Approach to the Study of Peripheral T-Cell Tolerance." Immunological Reviews 122, no. 1 (August 1991): 103–16. http://dx.doi.org/10.1111/j.1600-065x.1991.tb00599.x.

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Papatriantafyllou, M., G. Moldenhauer, J. Ludwig, A. Tafuri, N. Garbi, G. Hollmann, G. Kublbeck, et al. "Dickkopf-3, an immune modulator in peripheral CD8 T-cell tolerance." Proceedings of the National Academy of Sciences 109, no. 5 (January 17, 2012): 1631–36. http://dx.doi.org/10.1073/pnas.1115980109.

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Kouskoff, V. "T Cell-Independent Rescue of B Lymphocytes from Peripheral Immune Tolerance." Science 287, no. 5462 (March 31, 2000): 2501–3. http://dx.doi.org/10.1126/science.287.5462.2501.

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Journal articles on the topic 'Peripheral t cell tolerance'

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