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Relevant bibliographies by topics / Peripheral t cell tolerance

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Academic literature on the topic 'Peripheral t cell tolerance'

Author: Grafiati

Published: 4 June 2021

Last updated: 3 February 2022

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Journal articles on the topic "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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Dissertations / Theses on the topic "Peripheral t cell tolerance"

1

Blish, Catherine Anne. "Modulation of T cell function and T cell receptor repertoire during the induction of peripheral tolerance /." Thesis, Connect to this title online; UW restricted, 1999. http://hdl.handle.net/1773/8323.

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Jain, Nitya. "Multifaceted Regulation of Peripheral T Cell Tolerance and Autoimmunity by FOXP3+ T Regulatory Cells: A Dissertation." eScholarship@UMMS, 2009. https://escholarship.umassmed.edu/gsbs_diss/416.

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Adaptive immunity requires T cell responses to foreign pathogens to be counterbalanced with the need to limit collateral destruction of the host’s own tissues. Further, the presence of a substantial pool of lymphocytes capable of recognizing selfantigen in the periphery poses a threat to the maintenance of peripheral tolerance and prevention of autoimmunity. Regulatory T cells (Treg) that can suppress potentially self-reactive T cells are critical regulators of peripheral tolerance as well as initiation of immune responses. Treg cells employ several context-dependent mechanisms to establish regulation. In this thesis, we describe two distinct pathways of regulation used by Treg cells involving negative costimulation by CTLA-4 and immunomodulation by the morphogen, TGFβ. CTLA-4 is a co-inhibitory receptor on T cells essential for maintaining T cell homeostasis and tolerance to self. CTLA-4 expression is induced in conventional T cells following activation, whereas it is constitutively expressed in regulatory FOXP3+CD4+ regulatory T cells. Mice lacking CTLA-4 develop an early onset, fatal breakdown in T cell tolerance. Whether this autoimmune disease occurs because of the loss of CTLA-4 function in regulatory T cells, conventional T cells, or both, is not known. We present evidence here that in addition to a critical CTLA-4 function in regulatory T cells, CTLA-4 in conventional T cells is also necessary for controlling the consequences of abnormal T cell activation. CTLA-4 expression in activated conventional T cells only in vivois unable to compensate for the impaired function of CTLA-4-less regulatory T cells that results in systemic lymphoproliferation, but it can prevent the aberrantly activated T cells from infiltrating and fatally damaging non-lymphoid tissues. These results demonstrate that CTLA-4 has a dual function in maintaining T cell homeostasis: CTLA-4 in regulatory T cells inhibits inappropriate naïve T cell activation and CTLA-4 in conventional T cells can prevent the harmful accumulation of inappropriately activated pathogenic T cells in vital organs. In addition, we have identified Disabled-2 (Dab2), a TGFβ signaling intermediate, as a FOXP3 target gene that is expressed exclusively in Treg cells and is critical for in vitro and in vivo regulation by Treg cells. During T cell development, DAB2 is also expressed in a Foxp3-independent manner in thymic precursor cells, and acts as a sensor of TGFβ signals that is required for programming normal TGFβ responsiveness in T cell progenies. Naïve CD4+ T cells that differentiate from Dab2-deficient precursors favor Th17 cell generation at the expense of FOXP3+ Treg cells as a result of altered sensitivity to TGFβ. Importantly, retinoic acid can restore TGFβ signaling capacity of naïve CD4+ T cells generated from Dab2-deficient precursors, emphasizing the cooperative nature of retinoic acid and TGFβ signaling pathways in promoting Treg cell development and maintenance.

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Tunbridge, Helen. "Defining spatiotemporal patterns regulating T cell function in peripheral tolerance induction." Thesis, University of Bristol, 2016. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.691166.

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In the Tg4 murine model of multiple sclerosis, experimental autoimmune encephalomyelitis, disease burden can be reduced by repeated doses of self-peptide, resulting in the conversion of pathogenic T H1 cells into tolerant IL-10-secreting regulatory cells. This work sought to identify whether there are any differences in the spatiotemporal organisation of signalling intermediates in these two cell types using live cell imaging of T cells transduced with GFP-tagged signalling intermediates. Pattern classification of distributions found at the T:B cell interface was used to identify any altered localisation. The distribution of all sensors tested have already been established in a model of foreign antigen (5C.C7 transgenic mouse) and the function of these interface structures inferred from the roles of proteins that congregate there. Thus we can relate structure to function and better understand the effects of altered localisation of proteins in tolerance.

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Aksoylar, Halil I. "A Critical Role for Gimap5 in CD4+ T Cell Homeostasis and Maintenance of Peripheral Immune Tolerance." University of Cincinnati / OhioLINK, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1367937122.

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Divekar, Rohit Dilip Zaghouani Habib. "Two aspects of peripheral immune tolerance systemic and mucosal tolerance mechanisms /." Diss., Columbia, Mo. : University of Missouri-Columbia, 2008. http://hdl.handle.net/10355/6868.

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The entire dissertation/thesis text is included in the research.pdf file; the official abstract appears in the short.pdf file (which also appears in the research.pdf); a non-technical general description, or public abstract, appears in the public.pdf file. Title from PDF of title page (University of Missouri--Columbia, viewed on April 1, 2010). Vita. Thesis advisor: Habib Zaghouani. "May 2008" Includes bibliographical references.

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Yuschenkoff, Victoria Nicole. "Tolerance Induction to a Foreign Protein Antigen: Analysing the Role of B Cells in Establishing Peripheral Tolerance." eScholarship@UMMS, 1995. http://escholarship.umassmed.edu/gsbs_diss/298.

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Tolerance to self proteins is largely dependent upon the deletion of immature, self-specific T and B cells in the thymus and bone marrow. Although highly efficient, the elimination of these self-reactive lymphocytes is dependent on the expression of their target antigen in these primary lymphoid organs. Many proteins, however, such as hormones, are developmentally regulated and expressed at different stages of life, while other proteins are expressed outside the thymus and marrow. To ensure self-tolerance, other mechanisms must exist to inactivate or prevent the activation of mature, potentially self-reactive lymphocytes and maintain peripheral tolerance. T cell activation requires direct recognition of a specific protein fragment, presented on the surface of an antigen presenting cell (APC), as well as the interaction between various T cell and APC surface molecules. In the absence of the costimulatory signals provided by these ligand-pair interactions and lymphokines, antigen recognition leads to T cell inactivation and tolerance to the protein. Since many autoimmune disorders appear to be based upon the aberrant activation of mature T lymphocytes, it is important to identify and understand the mechanisms of peripheral tolerance. The obvious importance of the APC in initiating the T cell immune response has led our lab to examine one of the many antigen-processing cells, the B lymphocyte. Our studies have shown that B cells are highly efficient APC and can present antigen at very low doses to cultured T cell lines. In addition, we have found that we can induce tolerance, as measured by a reduced antibody response to an immunogenic form of the protein, in naive, normal mice by targeting a foreign protein to their B cells for antigen processing and presentation. Tolerance in the treated mice can be traced to a lesion in the T cell compartment of the animals, thus suggesting that B cells can act as tolerizing APC for peripherally expressed antigens. To further explore this idea and find more direct evidence for the role of B cells in establishing peripheral tolerance, we developed a model system that would more closely resemble in vivo conditions. This thesis tests and provides additional evidence for the hypothesis that B cells are tolerizing antigen presenting cells for peripherally expressed protein antigens. Tolerance to the foreign protein human μ chain, is induced in normal recipient mice by the transfusion of splenocytes from transgenic mice that express the membrane-bound form of μ on their B cells. Tolerance is antigen-specific since the transfused recipients' antibody production to the irrelevant protein chicken IgG is not compromised. Only viable transgenic spleen cells are tolerogenic and even when human μ chain is accessible to other APCs for presentation, tolerance can be induced by the transfusion of live μ transgenic splenoctyes. These data suggested that the transfused μ chain-expressing B cells are the tolerizing APCs which was confirmed by experiments that compared the tolerizing abilities of purified B and T cells from the transgenic mice. Adoptive transfer experiments showed that the recipients' T cell response to human μ was impaired but an analysis of the isotypes produced by tolerized mice did not indicate that either helper T cell subset was specifically compromised. Splenocytes from human μ chain-secreting transgenic B cells also induce tolerance to human μ in nontransgenic mice. Although human μ chain-expressing B cells were not detected in transfused mice, the presence of measurable levels of human IgM in the sera of mice transfused with μ chain-secreting spleen cells suggests that the transfused transgenic B cells persist in their new host. In addition, the tolerizing ability of both resting and activated membrane-bound μ chain B cells was compared. Lipopolysaccharide (LPS)-activated transgenic spleen cells do not tolerize, nor do they prime for antibody to human μ, thus suggesting that the induction of costimulatory molecules on the transgenic B cells inhibits tolerance induction. To more specifically address this, human μ chain-expressing mice were bred to transgenic mice that express the costimulatory molecule, B7-1 (CD80), on their B cells. Double transgenic splenocytes, in which the B cells bear both human μ and B7-1, did not induce tolerance to human μ chain, a result that supports the idea that activated B cells are not tolerogenic. Together the data in this thesis show that resting B cells can process and present a foreign endogenous antigen in a tolerogenic manner to the immune system and suggest a role for the B cell in the maintenance of peripheral tolerance.

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Wang, Lei [Verfasser], and Ludger [Akademischer Betreuer] Klein. "Mechanisms of central and peripheral T cell tolerance to an antigen of the central nervous system / Lei Wang ; Betreuer: Ludger Klein." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2017. http://d-nb.info/1128074060/34.

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Zheng, Xincheng. "Two-signal requirement for the development of T lymphocytes." Connect to this title online, 2005. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1109258062.

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Thesis (Ph. D.)--Ohio State University, 2005.
Title from first page of PDF file. Document formatted into pages; contains xvi, 156 p.; also includes graphics (some col.) Includes bibliographical references (p. 127-156). Available online via OhioLINK's ETD Center

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Falk, Johannes. "D-Aminosäuren-substituierte Peptidepitope induzierten T-Zell-Toleranz in vivo." Doctoral thesis, Humboldt-Universität zu Berlin, Medizinische Fakultät - Universitätsklinikum Charité, 2003. http://dx.doi.org/10.18452/14968.

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In dieser Arbeit wurde die Induktion spezifischer, immunologischer T-Zelltoleranz als therapeutische Strategie bei Autoimmunerkrankungen im Mausmodell untersucht. Da davon ausgegangen werden muss, dass viele der Autoimmunkrankheiten durch T-Zellen vermittelt sind, ist die Induktion spezifischer T-Zelltoleranz eine besonders interessante Therapiestrategie. Spezifische T-Zelltoleranz kann mittels Injektion des entsprechenden Peptidantigens induziert werden. Insgesamt sind zur Induktion einer solchen Toleranz, zumindest beim Menschen, relativ hohe Dosen an Peptidantigen notwendig. Die Produktion dieser Peptidantigene ist teuer. Bei unvorsichtiger Gabe kann es zur Anaphylaxie kommen. Es sollte also von Vorteil sein, die zu applizierende Menge an Peptid möglichst gering, dabei aber effizient zu halten. Vermutlich werden Antigene in Form von Peptiden schnell von unspezifischen Peptidasen und Proteasen in nicht-immunogene Fragmente gespalten und ausgeschieden, was wiederum eine hohe Dosierung erforderlich macht. Im Anfang der vorliegenden Arbeit stand die Hypothese, dass eine Stabilisierung des zu applizierenden Antigens zum Schutz vor Fragmentierung (und damit Wirkungsverlust) eine geeignete Methode sein könnte, Toleranzinduktion effektiver bzw. kostengünstiger zu gestalten. Bezüglich einer Stabilisierung von Peptiden zeigte sich, dass Peptide, welche aus rechtsdrehenden (D-)Aminosäuren zusammengesetzt sind, nur verzögert durch Proteasen/Peptidasen abgebaut werden. Wir setzten deshalb in dieser Arbeit D-Aninosäuren-substituierte Peptid-Varianten des Ovalbumin323-339-Peptidepitops (OVA323-339) ein und betrachteten die Wirkung dieser Peptide in vitro sowie in vivo auf spezifische DO11.10 T-Zellen. Basierend auf dem Peptidantigen OVA323-339, wurde zunächst ein minimales Epitop definiert, welches bei etwa gleicher Potenz um 6 Aminosäuren verkürzt werden konnte. Anschließend wurde eine Substitutionsanalyse durchgeführt, in der die ursprüngliche Aminosäuresequenz durch Austausch einiger L-Aminosäuren mittels D-Aminosäuren verändert wurde. Diese neu synthetisierten Peptide wurden zunächst auf ihre Fähigkeit überprüft, die OVA323-339 spezifischen DO11.10 T-Zellen in vitro zu aktivieren. Parallel konnte gezeigt werden, dass diese synthetisierten Peptidepitope in vitro eine deutlich verlängerte Serumhalbwertszeit aufwiesen. Im Weiteren wurde versucht, durch systemische Injektion von 300µg D-Peptid-Varianten in BABLB/c Mäusen T-Zelltoleranz zu induzieren. Die ex vivo restimulierten Lymphknoten-Zellen dieser Mäuse präsentierten je nach appliziertem Peptid eine reduzierte Proliferationsbereitschaft und IL-2 Sekretion. Die hier induzierte Toleranz konnte bis zu 60 Tagen post injectionem sowohl für das OVA323-339 als auch für einige der eingesetzten D-Peptide nachgewiesen werden. Auch nach Reduktion der Peptiddosis auf nur 100µg/Maus, waren die verkürzten und D-Aminosäuren-substituierten Peptide immer noch in der Lage sicher Toleranz zu induzieren. Die induzierte Toleranz durch D-Peptide war dabei der durch das Ausgangspeptid OVA323-339 induzierten Toleranz vergleichbar stark. Mit der Hilfe eines Transfermodells in unmanipulierte Mäuse, wurde das Verhalten der spezifischen T-Zellpopulation in vivo beobachtet. Durch den Transfer konnten in den Empfängermäusen (Balb/c) definierte T-Zellpopulationen bekannter Größe erzeugt werden. Mit dem Antikörper KJ1-26.1, der spezifisch den DO11.10-T-Zellrezeptor erkennt, konnten die transferierten Zellen in Geweben der Empfängermaus per FACS-Analyse nachgewiesen und deren Verhalten ex vivo studiert werden. Die intravenöse Injektion der serumstabilisierten Peptidanaloge führte in den transferierten Mäusen je nach Peptid zu einer funktionellen Nichtreaktivität (Anergie) als auch zur Deletion der für das Ausgangs(L-)Peptid spezifischen DO11.10 T-Zellen. In den oben genannten Versuchen ergaben sich Hinweise dafür, dass die D-Peptide ebenso effektiv sind wie das wesentlich längere Ausgangspeptid OVA323-339. Zukünftige Experimente werden weitere Aufschlüsse über einen möglichen Vorteil des Einsatzes von D-Peptiden in der Toleranzinduktion erbringen.
Induction of antigen-specific peripheral T cell tolerance in autoimmune diseases is an interesting therapeutically strategy. It can be induced by systemic injection of high-dose antigen. Investigations in induction of peripheral T cell tolerance in autoimmune mouse models revealed promising results. But it was also shown that the induced T cell tolerance spontaneously reverses after a period of time. This is probably due to a short in vivo half-life of the administrated peptide antigens. Since durable tolerance is required for this strategy to be of therapeutic value the administrated antigen-dose has to be of a very high and has to be injected repeatedly, and therefore bears an increased risk of anaphylactic reactions or exacerbation of the autoimmune disease. Because of these restrictions and also the high costs of peptide-production and purification, it is not surprising that this therapy didn t really find its way in to the clinical practice. The discovery that Peptides assembled partly or totally from D-amino acids are much more stable to proteolysis then natural L-peptides and therefore show an increased stability, lead to a wide interest of pharmacologists and immunologists. In former investigations it was shown that D-peptides used as vaccines elicited high levels of neutralizing antibodies so that there is no doubt about their immunogenic potency in vivo. It is also known that a single T cell receptor recognizes a wide range of peptide analogues that closely mimic the natural antigen. These observations led to our hypothesis, that the induction of peripheral T cell tolerance by systemic administration of D-Peptide substituted antigen variants should be possible and could be much more effective than the induction by the wild-type L-peptide. To verify our hypothesis we have chosen the well known OVA323-339 antigen which is recognized by T cells through the presentation in the I-Ad context. In a first step we performed a truncation analysis of OVA323-339 to identify a minimal epitope in it. We were able to demonstrate that the sequence OVA327-337 is as well potent as the original and 6 amino acids longer OVA323-339 sequence. The potency of new defined epitopes was tested by stimulating the OVA323-339 -specific DO11.10 T cells in vitro. In a stepwise performed substitution analysis we attempted to insert some D-amino acids in this novel peptide epitope. The DO11.10 cells only tolerated a few D-amino acid substitutions into the original sequence with the effect of now showing reduced proliferation. Performing an analysis of their half-life in vitro we identified two peptides as interesting candidates for the in vivo tolerance induction experiments. In the in vivo part of this work we induced peripheral tolerance by injecting the novel peptides into BALB/c mice. To monitor the behaviour of the tolerated T cells we also performed adoptive transfer experiments by transferring DO11.10 cells into naive BALB/c mice. With the help of the KJ26-1 antibody which specifically recognizes the DO11.10 T cell receptor it became possible to detect the transferred T cells ex vivo. Our results demonstrate that induction of peripheral T cell tolerance through injection of D-peptides is possible and long lasting (up to 60 days). Even with a dose reduction we found a stable T cell tolerance under ex vivo restimulation with the original peptide. Summarizing we were able to show that D-peptides are at least as effective as the natural occurring L-peptides inducing tolerance. Much more, the transfer experiments revealed that the kind of induced T cell tolerance (i.e. anergy and/or deletion through activation induced cell death) is antigen dependent and probably differs due to the agonistic potency of the given antigen.

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Chen, S. K. "Induction and maintenance of tolerance generated by temporary blockade of CD4 and CD8 on peripheral T cells in murine allo- and xenografts." Thesis, University of Cambridge, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.597534.

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Herein, I demonstrate that immunological tolerance can be induced in major histocompatibility complex (MHC) mismatched allogeneic heart and skin graft recipients and in concordant xenogeneic heart and skin graft recipients. Tolerance induction was achieved via temporary blockade of CD4 and CD8 co-signalling pathways mediated by non-depleting monoclonal antibodies. Basically, tolerance was demonstrated with four experimental models: 1) mouse heart allograft; 2) mouse skin allograft; 3) rat-to-mouse heart xenograft; and 4) rat-to-mouse skin xenograft. The tolerance induced to heart allograft was further investigated and was found to be specific, stable and transferable. The induced donor specific suppressive regulatory cells were CD4⁺: these could drive naive alloreactive cells to become new tolerant cells. Thus the population of tolerant cells can be numerically amplified via serial adoptive transfers. Tolerance may spread to linked antigens co-expressed with the original tolerogen. Tolerance, once established, was self perpetuating. To induce peripheral T cell tolerance, direct control of the pathway of T cell activation itself is more effective than control of the pathway of antigen presentation from antigen presentation from antigen presenting cells (APCs). Inhibition of direct antigen presentation via class II MHC had no effect on prolongation of allograft survival. Inhibition of indirect antigen presentation via class II MHC prolonged allograft survival, but did not lead to tolerance. AT cell may be activated to be aggressive, or suppressive, presumably depending upon their signal transduction at the time of antigen stimulation. Evidence provided here showed that the mature immune system can be reprogrammed to accept non-self organ graft as "self". Importantly the induced tolerance was an actively operational state. This is a demonstration that in principle, natural immune regulatory mechanisms may be exploited to induce permanent tolerance and may be developed for clinical use to avoid the need for prolonged immunosuppressive drug therapy.

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Books on the topic "Peripheral t cell tolerance"

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Schumacher, Paul Andrew. Biophysics and regulation of a whole-cell chloride current in human peripheral T lymphocytes. Ottawa: National Library of Canada, 1993.

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Peripheral T-cell immunological tolerance. Copenhagen: Munksgaard, 1993.

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O'Connor, Owen A., Won Seog Kim, and Pier L. Zinzani. Peripheral T-Cell Lymphomas. Wiley & Sons, Incorporated, John, 2020.

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O'Connor, Owen A., Won Seog Kim, and Pier L. Zinzani. Peripheral T-Cell Lymphomas. Wiley & Sons, Incorporated, John, 2020.

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O′Connor, Owen A., Won Seog Kim, and Pier L. Zinzani. Peripheral T-Cell Lymphomas. Wiley & Sons, Limited, John, 2020.

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Paolo Piccaluga, Pier, ed. Peripheral T-cell Lymphomas. IntechOpen, 2019. http://dx.doi.org/10.5772/intechopen.73947.

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O'Connor, Owen A., Won Seog Kim, and Pier Luigi Zinzani, eds. The Peripheral T‐Cell Lymphomas. Wiley, 2021. http://dx.doi.org/10.1002/9781119671336.

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

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Kiziroglu-Doganoglu, Fula. Tolerance induction at the CD4+ T helper precursor cell level in a veto-like manner. 1992.

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W, Alt Frederick, and Vogel Henry J. 1920-, eds. Molecular mechanisms of immunological self-recognition. San Diego: Academic Press, 1993.

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Book chapters on the topic "Peripheral t cell tolerance"

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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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van Parijs, Luk, Victor L. Perez, and Abul K. Abbas. "Mechanisms of Peripheral T Cell Tolerance." In Novartis Foundation Symposia, 5–20. Chichester, UK: John Wiley & Sons, Ltd., 2007. http://dx.doi.org/10.1002/9780470515525.ch2.

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Cameron, R., and L. Zhang. "T Cell Apoptosis and Its Role in Peripheral Tolerance." In Apoptosis and Its Modulation by Drugs, 179–96. Berlin, Heidelberg: Springer Berlin Heidelberg, 2000. http://dx.doi.org/10.1007/978-3-642-57075-9_7.

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Arnold, Bernd, Günther Schönrich, Iris Ferber, Judith Alferink, and Günter J. Hämmerling. "Tolerance induction in mature peripheral T cells." In Autoimmunity: Experimental Aspects, 1–9. Berlin, Heidelberg: Springer Berlin Heidelberg, 1994. http://dx.doi.org/10.1007/978-3-642-78779-9_1.

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Venuprasad, K. "Signaling Pathways of Cbl-b and Its Role in Peripheral T Cell Tolerance." In Trends in Stem Cell Proliferation and Cancer Research, 195–203. Dordrecht: Springer Netherlands, 2013. http://dx.doi.org/10.1007/978-94-007-6211-4_8.

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Tada, T., S. Kubo, and T. Nakayama. "Self-Tolerance: Multiple Strategies for Peripheral Unresponsiveness of T Cells." In New Trends in Allergy IV, 359–64. Berlin, Heidelberg: Springer Berlin Heidelberg, 1997. http://dx.doi.org/10.1007/978-3-642-60419-5_63.

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Allison, James P., Cynthia Chambers, Arthur Hurwitz, Tim Sullivan, Brigitte Boitel, Sylvie Fournier, Monika Brunner, and Matthew Krummel. "A Role for CTLA-4-Mediated Inhibitory Signals in Peripheral T Cell Tolerance?" In Novartis Foundation Symposia, 92–102. Chichester, UK: John Wiley & Sons, Ltd., 2007. http://dx.doi.org/10.1002/9780470515525.ch7.

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Parker, David C. "Peripheral Tolerance." In T Lymphocytes, 61–69. Boston, MA: Springer US, 1992. http://dx.doi.org/10.1007/978-1-4615-3054-1_6.

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Kuschnaroff, L. M., K. De Belder, M. Vandeputte, and M. Waer. "Factors involved in peripheral T cell tolerance: the extent of clonal deletion or clonal anergy depends on the age of the tolerized lymphocytes." In Transplant International Official Journal of the European Society for Organ Transplantation, 589–93. Berlin, Heidelberg: Springer Berlin Heidelberg, 1992. http://dx.doi.org/10.1007/978-3-642-77423-2_172.

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Pape, Kathryn A., Alex Khoruts, Elizabeth Ingulli, Anna Mondino, Rebecca Merica, and Marc K. Jenkins. "Antigen-Specific CD4+ T Cells that Survive after the Induction of Peripheral Tolerance Possess an Intrinsic Lymphokine Production Defect." In Novartis Foundation Symposia, 103–19. Chichester, UK: John Wiley & Sons, Ltd., 2007. http://dx.doi.org/10.1002/9780470515525.ch8.

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Conference papers on the topic "Peripheral t cell tolerance"

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Laginestra, Maria Antonella, Fabio Fuligni, Maura Rossi, Davide Gibellini, Maria Rosaria Sapienza, Anna Gazzola, Claudia Mannu, et al. "Abstract 5275: miRNA profiling of peripheral T-cell lymphomas." 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.am2013-5275.

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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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Horwitz, Steven M. "Abstract IA21: Biomarker-informed studies in peripheral T-cell lymphoma." In Abstracts: AACR Virtual Meeting: Advances in Malignant Lymphoma; August 17-19, 2020. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/2643-3249.lymphoma20-ia21.

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Crouser, ED, MW Julian, G. Shao, C. Fox, D. Hauswirth, J. Jehn, G. Lozanski, S. Erdal, and MD Wewers. "Infliximab Reverses Peripheral CD4+ T Cell Depletion in Lymphopenic Sarcoidosis Patients." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a2255.

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Simpson, Haley M., Aki Furusawa, Kavitha Sadashivaiah, and Arnob Banerjee. "Abstract 363: STAT5 inhibition induces apoptosis in peripheral T cell lymphoma." 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.am2017-363.

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Schott, Cody, Christian Ascoli, Yue Huang, David Perkins, and Patricia Finn. "Diminished peripheral T cell activity in sarcoidosis associates with progressive disease." In ERS International Congress 2018 abstracts. European Respiratory Society, 2018. http://dx.doi.org/10.1183/13993003.congress-2018.oa2156.

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Rana, Seema, and Rajiv Tangri. "Anaplastic large cell lymphoma ALK negative vs. peripheral T cell lymphoma (NOS) - diagnostic dilemma." In 16th Annual International Conference RGCON. Thieme Medical and Scientific Publishers Private Ltd., 2016. http://dx.doi.org/10.1055/s-0039-1685354.

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Abstract:

Middle aged female presented with generalised lymphadenopathy and fever for last one month. Peripheral blood findings were within normal limits. There was no extra nodal involvement. FNAC performed initially from a cervical node suggested possibility of Hodgkin’s lymphoma and a whole node biopsy was performed. Histopathogical examination revealed effaced nodal architecture and a polymorphous population of lymphocytes, plasma cells, neutrophils and scattered large mononuclear cells with prominent nucleolus. An initial panel of CD3, CD20, LCA, CD15, CD30 and PAX5 was performed. The large atypical cells were positive for LCA, CD3 and CD30 with variable positivity for CD15. CD 30 showed Golgi and membranous staining. These large atypical cells were negative for PAX5 and CD20. In view of above findings, Hodgkin’s lymphoma was ruled out and a possibility of Non- Hodgkin’s lymphoma was considered. Further IHC markers were performed which included CD2, CD5, CD7, EMA, Alk, CD10 and KI67. CD5 showed variable positivity. The cells of interest were negative for CD2, CD7, ALK and EMA. Ki 67 index was 70-80%. Overall histological and IHC findings favoured Alk negative Anaplastic large cell lymphoma. Differential diagnosis considered was peripheral T cell lymphoma (NOS). Hodgkin’s lymphoma, peripheral T cell lymphoma (NOS) and anaplastic large cell lymphoma share common histomorphological findings. With careful analysis of Immunohistochemistry, it is easier to categorise Hodgkin’s lymphoma. ALK negative anaplastic large cell lymphoma and peripheral T cell lymphoma (NOS) are difficult to categorise and show overlapping features. We in this case have discussed clinical, histomorphological and IHC pattern of Alk negative Anaplastic large cell lymphoma.

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Wu, Yang, Dan Chen, Rong Ma, Jun-ying Zhang, Yuan Zhang, Hai-xia Cao, Zhuo Wang, et al. "Abstract 1444: The new therapy strategy for treatment of peripheral T cell lymphomas: CD30-targeted CAR-modified T cell therapy." 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.am2019-1444.

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Wu, Yang, Dan Chen, Rong Ma, Jun-ying Zhang, Yuan Zhang, Hai-xia Cao, Zhuo Wang, et al. "Abstract 1444: The new therapy strategy for treatment of peripheral T cell lymphomas: CD30-targeted CAR-modified T cell therapy." 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.sabcs18-1444.

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Reports on the topic "Peripheral t cell tolerance"

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Gray, Andrew. Enhancing the Efficacy of Prostate Cancer Immunotherapy by Manipulating T-Cell Receptor Signaling in Order to Alter Peripheral Regulatory T-Cell Activity. Fort Belvoir, VA: Defense Technical Information Center, July 2009. http://dx.doi.org/10.21236/ada511997.

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Gray, Andrew. Enhancing the Efficacy of Prostate Cancer Immunotherapy by Manipulating T-Cell Receptor Signaling in Order to Alter Peripheral Regulatory T-Cell Activity. Fort Belvoir, VA: Defense Technical Information Center, July 2011. http://dx.doi.org/10.21236/ada553485.

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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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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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