Relevant bibliographies by topics / Antigen tolerance

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

Academic literature on the topic 'Antigen tolerance'

Author: Grafiati
Published: 4 June 2021
Last updated: 11 February 2022

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Journal articles on the topic "Antigen tolerance"

1

Oehen, S., L. Feng, Y. Xia, C. D. Surh, and S. M. Hedrick. "Antigen compartmentation and T helper cell tolerance induction." Journal of Experimental Medicine 183, no. 6 (June 1, 1996): 2617–26. http://dx.doi.org/10.1084/jem.183.6.2617.

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The process of antigen recognition depends in part on the amount of peptide antigen available and the affinity of the T cell receptor for a particular peptide-major histocompatibility complex (MHC) molecule complex. The availability of self antigen is limited by antigen processing, which is compartmentalized such that peptide antigens presented by MHC class I molecules originate in the cytoplasm, whereas peptide antigens presented by MHC class II molecules are acquired from the endocytic pathway. This segregation of the antigen-processing pathways may limit the diversity of antigens that influence the development and selection of, e.g., CD4-positive, MHC class II-specific T cells. Selection in this case might involve only a subset of self-encoded proteins, specifically those that are plasma membrane bound or secreted. To study these aspects of immune development, we engineered pigeon cytochrome for expression in transgenic mice in two forms: one in which it was expressed as a type II plasma membrane protein, and a second in which it was targeted to the mitochondria after cytoplasmic synthesis. Experiments with these mice clearly show that tolerance is induced in the thymus, irrespective of antigen compartmentation. Using radiation bone marrow chimeras, we further show that cytoplasmic/mitochondrial antigen gains access to the MHC class II pathway by direct presentation. As a result of studying the anatomy of the thymus, we show that the amount of antigen and the affinity of the TCR affect the location and time point of thymocytes under-going apoptosis.
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Carmona, Priscila, Yordanka Medina-Armenteros, Amanda Cabral, Sandra Maria Monteiro, Simone Gonçalves Fonseca, Ana Caetano Faria, Francine Lemos, et al. "Regulatory/inflammatory cellular response discrimination in operational tolerance." Nephrology Dialysis Transplantation 34, no. 12 (July 5, 2019): 2143–54. http://dx.doi.org/10.1093/ndt/gfz114.

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Abstract Background Antigen-specific cellular response is essential in immune tolerance. We tested whether antigen-specific cellular response is differentially modulated in operational tolerance (OT) in renal transplantation with respect to critical antigenic challenges in allotransplantation—donor antigens, pathogenic antigens and self-antigens. Methods We analysed the profile of immunoregulatory (REG) and pro-inflammatory (INFLAMMA) cytokines for the antigen-specific response directed to these three antigen groups, by Luminex. Results We showed that, in contrast to chronic rejection and healthy individuals, OT gives rise to an immunoregulatory deviation in the cellular response to donor human leucocyte antigen DR isotype peptides, while preserving the pro-inflammatory response to pathogenic peptides. Cellular autoreactivity to the N6 heat shock protein 60 (Hsp60) peptide also showed a REG profile in OT, increasing IL4, IL-5, IL-10 and IL-13. Conclusions The REG shift of donor indirect alloreactivity in OT, with inhibition of interleukin (IL)-1B, IL-8, IL-12, IL-17, granulocyte colony-stimulating factor, Interferon-γ and monocyte chemoattractant protein-1, indicates that this may be an important mechanism in OT. In addition, the differential REG profile of cellular response to the Hsp60 peptide in OT suggests that REG autoimmunity may also play a role in human transplantation tolerance. Despite cross-reactivity of antigen-specific T cell responses, a systemic functional antigen-specific discrimination takes place in OT.
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Taylor, Justin J., Ryan J. Martinez, Philip J. Titcombe, Laura O. Barsness, Stephanie R. Thomas, Na Zhang, Shoshana D. Katzman, Marc K. Jenkins, and Daniel L. Mueller. "Deletion and anergy of polyclonal B cells specific for ubiquitous membrane-bound self-antigen." Journal of Experimental Medicine 209, no. 11 (October 15, 2012): 2065–77. http://dx.doi.org/10.1084/jem.20112272.

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B cell tolerance to self-antigen is critical to preventing antibody-mediated autoimmunity. Previous work using B cell antigen receptor transgenic animals suggested that self-antigen–specific B cells are either deleted from the repertoire, enter a state of diminished function termed anergy, or are ignorant to the presence of self-antigen. These mechanisms have not been assessed in a normal polyclonal repertoire because of an inability to detect rare antigen-specific B cells. Using a novel detection and enrichment strategy to assess polyclonal self-antigen–specific B cells, we find no evidence of deletion or anergy of cells specific for antigen not bound to membrane, and tolerance to these types of antigens appears to be largely maintained by the absence of T cell help. In contrast, a combination of deleting cells expressing receptors with high affinity for antigen with anergy of the undeleted lower affinity cells maintains tolerance to ubiquitous membrane-bound self-antigens.
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Chung, Yeonseok, Jae-Hoon Chang, Mi-Na Kweon, Paul D. Rennert, and Chang-Yuil Kang. "CD8α–11b+ dendritic cells but not CD8α+ dendritic cells mediate cross-tolerance toward intestinal antigens." Blood 106, no. 1 (July 1, 2005): 201–6. http://dx.doi.org/10.1182/blood-2004-11-4240.

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Cross-presentation is a critical process by which antigen is displayed to CD8 T cells to induce tolerance. It is believed that CD8α+ dendritic cells (DCs) are responsible for cross-presentation, suggesting that the CD8α+ DC population is capable of inducing both cross-priming and cross-tolerance to antigen. We found that cross-tolerance against intestinal soluble antigen was abrogated in C57BL/6 mice lacking mesenteric lymph nodes (MLNs) and Peyer patches (PPs), whereas mice lacking PPs alone were capable of developing CD8 T-cell tolerance. CD8α–CD11b+ DCs but not CD8α+ DCs in the MLNs present intestinal antigens to relevant CD8 T cells, while CD8α+ DCs but not CD8α–CD11b+ DCs in the spleen exclusively cross-present intravenous soluble antigen. Thus, CD8α–CD11b+ DCs in the MLNs play a critical role for induction of cross-tolerance to dietary proteins.
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Duong, Bao Hoa, Hua Tian, Takayuki Ota, Gladys Completo, Shoufa Han, José Luis Vela, Miyo Ota, et al. "Decoration of T-independent antigen with ligands for CD22 and Siglec-G can suppress immunity and induce B cell tolerance in vivo." Journal of Experimental Medicine 207, no. 1 (December 28, 2009): 173–87. http://dx.doi.org/10.1084/jem.20091873.

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Autoreactive B lymphocytes first encountering self-antigens in peripheral tissues are normally regulated by induction of anergy or apoptosis. According to the “two-signal” model, antigen recognition alone should render B cells tolerant unless T cell help or inflammatory signals such as lipopolysaccharide are provided. However, no such signals seem necessary for responses to T-independent type 2 (TI-2) antigens, which are multimeric antigens lacking T cell epitopes and Toll-like receptor ligands. How then do mature B cells avoid making a TI-2–like response to multimeric self-antigens? We present evidence that TI-2 antigens decorated with ligands of inhibitory sialic acid–binding Ig-like lectins (siglecs) are poorly immunogenic and can induce tolerance to subsequent challenge with immunogenic antigen. Two siglecs, CD22 and Siglec-G, contributed to tolerance induction, preventing plasma cell differentiation or survival. Although mutations in CD22 and its signaling machinery have been associated with dysregulated B cell development and autoantibody production, previous analyses failed to identify a tolerance defect in antigen-specific mutant B cells. Our results support a role for siglecs in B cell self-/nonself-discrimination, namely suppressing responses to self-associated antigens while permitting rapid “missing self”–responses to unsialylated multimeric antigens. The results suggest use of siglec ligand antigen constructs as an approach for inducing tolerance.
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Jung, Kyeong Cheon, Chung-Gyu Park, Yoon Kyung Jeon, Hyo Jin Park, Young Larn Ban, Hye Sook Min, Eun Ji Kim, et al. "In situ induction of dendritic cell–based T cell tolerance in humanized mice and nonhuman primates." Journal of Experimental Medicine 208, no. 12 (October 24, 2011): 2477–88. http://dx.doi.org/10.1084/jem.20111242.

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Induction of antigen-specific T cell tolerance would aid treatment of diverse immunological disorders and help prevent allograft rejection and graft versus host disease. In this study, we establish a method of inducing antigen-specific T cell tolerance in situ in diabetic humanized mice and Rhesus monkeys receiving porcine islet xenografts. Antigen-specific T cell tolerance is induced by administration of an antibody ligating a particular epitope on ICAM-1 (intercellular adhesion molecule 1). Antibody-mediated ligation of ICAM-1 on dendritic cells (DCs) led to the arrest of DCs in a semimature stage in vitro and in vivo. Ablation of DCs from mice completely abrogated anti–ICAM-1–induced antigen-specific T cell tolerance. T cell responses to unrelated antigens remained unaffected. In situ induction of DC-mediated T cell tolerance using this method may represent a potent therapeutic tool for preventing graft rejection.
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Feng, Xiangru, Jiaxue Liu, Weiguo Xu, Gao Li, and Jianxun Ding. "Tackling autoimmunity with nanomedicines." Nanomedicine 15, no. 16 (July 2020): 1585–97. http://dx.doi.org/10.2217/nnm-2020-0102.

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Tolerogenic immunotherapy aims to blunt pathogenic inflammation without affecting systemic immunity. However, the anti-inflammatory drugs and immunosuppressive biologics that are used in the clinic usually result in nonspecific immune cell suppression and off-target toxicity. For this reason, strategies have been developed to induce antigen-specific immune tolerance through the delivery of disease-relevant antigens by nanocarriers as a benefit of their preferential internalization by antigen-presenting cells. Herein, we discuss the recent advances in the nanotechnology-based antigen-specific tolerance approaches. Some of these designs are based on nanoparticles delivering antigens and immunoregulatory agents to modulate antigen-presenting pathways, while others directly target T cells via nanoparticle-based artificial antigen-presenting cells. These antigen-specific therapies are hoped to replace systemic immune suppression and provide long-term disease remission.
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Mapara, Markus Y., and Megan Sykes. "Tolerance and Cancer: Mechanisms of Tumor Evasion and Strategies for Breaking Tolerance." Journal of Clinical Oncology 22, no. 6 (March 15, 2004): 1136–51. http://dx.doi.org/10.1200/jco.2004.10.041.

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The development of malignant disease might be seen as a failure of immune surveillance. However, not all tumors are naturally immunogenic, and even among those that are immunogenic, the uncontrolled rapid growth of a tumor may sometimes out-run a robust immune response. Nevertheless, recent evidence suggests that mechanisms of tolerance that normally exist to prevent autoimmune disease may also preclude the development of an adequate antitumor response and that tumors themselves have the ability to thwart the development of effective immune responses against their antigens. A major challenge has been to develop approaches to breaking this tolerance in tumor-bearing hosts, and recent advances in our understanding of antigen presentation and tolerance have led to some promising strategies. An alternative approach is to use T cells from nontumor-bearing, allogeneic hosts in the form of lymphocyte infusions, with or without hematopoietic cell transplantation. Immunotherapy may occur in this setting via the response of nontolerant, tumor antigen-specific T cells from nontumor-bearing hosts or via the powerful destructive effect of an alloresponse directed against antigens shared by malignant cells in the recipient. Approaches to exploiting this beneficial effect without the deleterious consequence of graft-versus-host disease in allogeneic hematopoietic cell recipients are discussed.
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Horst, Andrea Kristina, Kingsley Gideon Kumashie, Katrin Neumann, Linda Diehl, and Gisa Tiegs. "Antigen presentation, autoantibody production, and therapeutic targets in autoimmune liver disease." Cellular & Molecular Immunology 18, no. 1 (October 27, 2020): 92–111. http://dx.doi.org/10.1038/s41423-020-00568-6.

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AbstractThe liver is an important immunological organ that controls systemic tolerance. The liver harbors professional and unconventional antigen-presenting cells that are crucial for tolerance induction and maintenance. Orchestrating the immune response in homeostasis depends on a healthy and well-toned immunological liver microenvironment, which is maintained by the crosstalk of liver-resident antigen-presenting cells and intrahepatic and liver-infiltrating leukocytes. In response to pathogens or autoantigens, tolerance is disrupted by unknown mechanisms. Intrahepatic parenchymal and nonparenchymal cells exhibit unique antigen-presenting properties. The presentation of microbial and endogenous lipid-, metabolite- and peptide-derived antigens from the gut via conventional and nonconventional mechanisms can educate intrahepatic immune cells and elicit effector responses or tolerance. Perturbation of this balance results in autoimmune liver diseases, such as autoimmune hepatitis, primary biliary cholangitis, and primary sclerosing cholangitis. Although the exact etiologies of these autoimmune liver diseases are unknown, it is thought that the disruption of tolerance towards self-antigens and microbial metabolites and lipids, as well as alterations in bile acid composition, may result in changes in effector cell activation and polarization and may reduce or impair protective anti-inflammatory regulatory T and B cell responses. Additionally, the canonical and noncanonical transmission of antigens and antigen:MHC complexes via trogocytosis or extracellular vesicles between different (non) immune cells in the liver may play a role in the induction of hepatic inflammation and tolerance. Here, we summarize emerging aspects of antigen presentation, autoantibody production, and the application of novel therapeutic approaches in the characterization and treatment of autoimmune liver diseases.
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Parks, Christopher A., Kalli R. Henning, Kevin D. Pavelko, Michael J. Hansen, Virginia P. Van Keulen, Brendan K. Reed, Jennifer D. Stone, et al. "Breaking tolerance with engineered class I antigen-presenting molecules." Proceedings of the National Academy of Sciences 116, no. 8 (February 6, 2019): 3136–45. http://dx.doi.org/10.1073/pnas.1807465116.

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Successful efforts to activate T cells capable of recognizing weak cancer-associated self-antigens have employed altered peptide antigens to activate T cell responses capable of cross-reacting on native tumor-associated self. A limitation of this approach is the requirement for detailed knowledge about the altered self-peptide ligands used in these vaccines. In the current study we considered allorecognition as an approach for activating CTL capable of recognizing weak or self-antigens in the context of self-MHC. Nonself antigen-presenting molecules typically contain polymorphisms that influence interactions with the bound peptide and TCR interface. Recognition of these nonself structures results in peptide-dependent alloimmunity. Alloreactive T cells target their inducing alloantigens as well as third-party alloantigens but generally fail to target self-antigens. Certain residues located on the alpha-1/2 domains of class I antigen-presenting molecules primarily interface with TCR. These residues are more conserved within and across species than are residues that determine peptide antigen binding properties. Class I variants designed with amino acid substitutions at key positions within the conserved helical structures are shown to provide strong activating signals to alloreactive CD8 T cells while avoiding changes in naturally bound peptide ligands. Importantly, CTL activated in this manner can break self-tolerance by reacting to self-peptides presented by native MHC. The ability to activate self-tolerant T cells capable of cross-reacting on self-peptide-MHC in vivo represents an approach for inducing autoimmunity, with possible application in cancer vaccines.
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Dissertations / Theses on the topic "Antigen tolerance"

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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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Chen, Tse-Ching. "Dominant tolerance to a minor histocompatibility antigen." Thesis, University of Oxford, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.400052.

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Whitley, Nathaniel T. "Mechanisms in antigen-specific tolerance induction therapy." Thesis, University of Bristol, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.411069.

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Matriano, James Abcede. "Peripheral tolerance to an organ-specific antigen." Case Western Reserve University School of Graduate Studies / OhioLINK, 1991. http://rave.ohiolink.edu/etdc/view?acc_num=case1059484721.

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Ferry, Helen. "B cell tolerance to systemic, intracellular self-antigen." Thesis, University of Oxford, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.442947.

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Marshall, Naomi Jane. "Antigen presentation in autoimmune disease." Thesis, University of Edinburgh, 2009. http://hdl.handle.net/1842/4212.

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The aim of my project was to examine the extent to which endogenous expression of a largely renal-specific antigen influences the repertoire in adulthood of autoreactive T cells specific to that antigen. The renal-specific antigen, human α3(IV)NC1, is the target of autoimmune attack in Goodpasture’s disease. This protein was expressed and purified in recombinant (using bacterial and mammalian cell expression systems) and purified in native (extracted from human tissue) forms. Transgenic mice were generated that express HLA-DR15 (associated with Goodpasture’s disease) as their sole MHC class II molecule, and for which α3(IV)NC1 can be endogenous or exogenous. The CD4 T cell responses of these mice were then tested following immunisation with α3(IV)NC1. In mice with endogenous expression of α3(IV)NC1 there were no consistent detectable proliferative T cell responses to any α3(IV)NC1 peptides in a set of overlapping peptides representative of the entire sequence. In the mice lacking endogenous α3(IV)NC1 there were consistent responses to the peptide α3(IV)NC1 136-150. This contains part of the peptide recognised by the most abundant autoreactive T cells in patients with acute Goodpasture’s disease. Therefore, the T cell responses seen in man to an endogenous (auto)antigen have similar fine specificity to those seen in mice responding to the same protein as a foreign antigen. This is surprising as one might expect self-tolerance in man to be most secure to such dominantly presented and immunogenic (in HLA DR15 mice) self peptides. However, recent work suggests that the peptide most commonly presented in humans is normally destroyed during antigen processing, giving a possible explanation for the lack of tolerance. Future work should study why tolerance is ineffective to this particular peptide, whether tolerance can be reinforced, these questions could be addressed using a transgenic mouse model that develops Goodpasture-like pathology. In addition, how processing is defective in Goodpasture’s disease could be explored by making antigen presenting hybridomas from patient samples or from the transgenic mouse line described within this thesis.
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Wheeler, Paul Richard. "Characterisation of T cell anergy in allo-antigen specific CD4⁺ cells." Thesis, University of Oxford, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.288516.

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Konkel, Joanne Elizabeth. "Signals required for the induction of antigen-based therapeutic tolerance." Thesis, University of Edinburgh, 2009. http://hdl.handle.net/1842/3942.

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Despite the actions of central tolerance during thymic selection, it is clear that the peripheral T cell repertoire contains significant numbers of self-reactive T cells. The immune system needs to curtail the risk of autoimmune disease by controlling the activity of these self-reactive T cells. Various mechanisms are in place to achieve this control (peripheral tolerance). Activation of CD4+ T cells requires two signals; engagement of the T cell receptor (TCR) with an appropriate peptide:MHC complex (signal 1), and the aggregate effect of multiple signals generated following ligation of costimulatory and coinhibitory molecules (signal 2). Both signals are required for the generation of a productive T cell response and both are provided by the professional antigen presenting cell, the dendritic cell (DC). T cells are fully activated upon receiving both signal 1 and 2, but are rendered tolerant when they receive only signal 1. This can be exploited therapeutically through the administration of peptides to induce tolerance in peptidereactive T cells. Administration of peptide with an adjuvant provides both signal 1 and 2, and leads to a sustained T cell response against the administered peptide (immunity). However, if the same peptide is administered in soluble form, only signal 1 is provided, leading to the establishment of T cell tolerance. The studies in this thesis explore the role of both signal 1 and signal 2 in peptide-induced T cell tolerance. Previous data from our laboratory have highlighted PD-1 and RANKL as costimulatory molecules which could play a role in peptide-induced T cell tolerance. Here we show that PD-1, an important coinhibitory molecule, plays a vital role in restraining peripheral T cell expansion under conditions leading to T cell immunity. However, in contrast to data from other studies, we demonstrate that PD-1 plays no role in the induction, establishment or maintenance of peptide-induced T cell tolerance. We show that the costimulatory receptor ligand pair RANK:RANKL plays a role in the balance between T cell tolerance and immunity; as administration of anti-RANKL was seen to potentiate both tolerance and immunity. We also explored the effect of altering the affinity of a peptide for MHC on the induction of peptide tolerance. We demonstrate that use of a peptide with a high-affinity for MHC induces tolerance via a novel, non-deletional mechanism of peptide-tolerance induction. Importantly, we show that the high-affinity peptide can form peptide- MHC complexes which persist in a biologically relevant form for fourteen days following peptide administration. We suggest that this leads to chronic stimulation of peptide-reactive T cells which promotes acquisition of a novel tolerant phenotype. Collectively the work described in this thesis demonstrates the important roles both signal 1 and 2 play in therapeutic-tolerance induction and how the qualitative and quantitative alteration of these signals can alter T cell fate and/or responsiveness.
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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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Sefia, Eseberuo. "Mechanism of immune tolerance induction in antigen-specific human autoimmune disease." Thesis, Queen Mary, University of London, 2014. http://qmro.qmul.ac.uk/xmlui/handle/123456789/8982.

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Multiple sclerosis (MS) is an inflammatory disease that affects the central nervous system and is considered to be a T-cell mediated autoimmune disease. The “ideal” method in treating MS would be an antigen-specific therapy that does not require generalized immunosuppression. To date there are no definitive treatments for MS but there are several licensed therapies such as -interferon. Unfortunately the effect of interferon (IFN) is reduced by the development of neutralizing antibodies (NAbs) in up to 35% of MS patients within two years of starting treatment. An immunization schedule was developed in the BALB/c mice by subcutaneous administration of recombinant human IFN, and this resulted in development of high incidence of NAbs to the protein in the BALB/c model termed “NAbs model”. The mechanism of NAbs formation in this model is believed to be similar to that observed in IFN-treated MS patients with NAbs, which is as a result of an immune response to the protein. We elected to study NAbs in the context of IFN rather than MS directly to investigate the effects of antigen-specific tolerization strategies on the outcome of NAbs and indirectly on the outcome of IFN treatment in MS disease. The depletion of the immune cells triggers a reconstitution program that leads to renewal of the immune cell repertoire. Tolerance can be induced by intravenous administration of a protein. Within this window of reconstitution following depletion, it is hoped that the immune system can be manipulated to tolerate an otherwise foreign protein (human recombinant IFN). The tolerance strategy employed in this project was immune cell depletion using antibodies and mitoxantrone, followed by intravenous re-introduction of rhIFN. Tolerance was successfully induced in the NAbs model by intravenous administration of rhIFN, and further enhanced by immune cell depletion prior to intravenous administration of rhIFN. The BALB/c “NAbs model” offers a suitable model for use in investigating induction of tolerance to rhIFN following the formation of NAbs to the protein. The antigen of interest is known and the time to NAbs formation is also known. Tolerance induction can be monitored and investigated in this model.
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Books on the topic "Antigen tolerance"

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Teng, Yen-Tung Andy. Analysis of the mechanism(s) of immunological tolerance to a physiological soluble antigen in transgenic mice. Ottawa: National Library of Canada = Bibliothèque nationale du Canada, 1997.

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Morteau, Olivier. Oral tolerance: The response of the intestinal mucosa to dietary antigens. Georgetown, Tex: Landes Bioscience/Eurekah.com, 2004.

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Morteau, Olivier. Oral tolerance: The response of the intestinal mucosa to dietary antigens. Georgetown, Tex: Landes Bioscience/Eurekah.com, 2004.

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Morteau, Olivier. Oral tolerance: The response of the intestinal mucosa to dietary antigens. Georgetown, TX: Landes Bioscience, 2001.

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Razzaghi, Hamid. Establishment of transgenic mice carrying mutated human insulin gene: A model system for studying the immunological self-tolerance to a soluble antigen. Ottawa: National Library of Canada, 1993.

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EMBO, Workshop on Tolerance (1986 Basel Switzerland). The tolerance workshop: Proceedings of the EMBO Workshop on Tolerance held at the Basel Institute for Immunology, 20-26 October 1986. Basle: Editiones Roche, 1987.

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I, Johnston Paul, ed. Anthology of the theological writings of J. Michael Reu. Lewiston: E. Mellen Press, 1997.

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Morteau, Olivier. Oral Tolerance: The Response of the Intestinal Mucosa to Dietary Antigens. Springer, 2010.

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Morteau, Olivier. Oral Tolerance: Cellular and Molecular Basis, Clinical Aspects, and Therapeutic Potential (Medical Intelligence Unit). Springer, 2004.

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(Editor), B. Kyewski, and Elisabeth Suri-Payer (Editor), eds. CD4+CD25+ Regulatory T Cells: Origin, Function and Therapeutic Potential (Current Topics in Microbiology and Immunology). Springer, 2005.

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Book chapters on the topic "Antigen tolerance"

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Stoy, Nicholas S. "Macrophages - Balancing Tolerance and Immunity." In Antigen Presenting Cells, 331–414. Weinheim, FRG: Wiley-VCH Verlag GmbH & Co. KGaA, 2006. http://dx.doi.org/10.1002/3527607021.ch10.

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McGeachy, Mandy J., Richard O’Connor, Leigh A. Stephens, and Stephen M. Anderton. "Antigen-Based Therapy and Immune-Regulation in Experimental Autoimmune Encephalomyelitis." In Immunological Tolerance, 313–26. Totowa, NJ: Humana Press, 2007. http://dx.doi.org/10.1007/978-1-59745-395-0_18.

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de Heusch, Magali, Guillaume Oldenhove, and Muriel Moser. "Dendritic Cells (DCs) in Immunity and Maintenance of Tolerance." In Antigen Presenting Cells, 503–22. Weinheim, FRG: Wiley-VCH Verlag GmbH & Co. KGaA, 2006. http://dx.doi.org/10.1002/3527607021.ch14.

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McBride, J. S. "From Serology of the Chicken MHC to Polymorphism of Malaria Antigen Genes." In Realm of Tolerance, 154–59. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-74712-0_18.

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Bruce, M. G., and A. Ferguson. "Oral Tolerance Induced by Gut-Processed Antigen." In Recent Advances in Mucosal Immunology, 721–31. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4684-5344-7_84.

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Kretschmer, Karsten, Irina Apostolou, Panos Verginis, and Harald von Boehmer. "Regulatory T Cells and Antigen-Specific Tolerance." In Chemical Immunology and Allergy, 8–15. Basel: KARGER, 2008. http://dx.doi.org/10.1159/000154846.

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Zheng, Lixin, Stefen A. Boehme, Jeffrey M. Critchfield, Juan Carlos Zuniga-Pflucker, Matthew Freedman, and Michael J. Lenardo. "Immunological Tolerance by Antigen-Induced Apoptosis of Mature T Lymphocytes." In Advances in Experimental Medicine and Biology, 81–89. Boston, MA: Springer US, 1994. http://dx.doi.org/10.1007/978-1-4899-0987-9_9.

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Woods, David M., Andressa Laino, Alejandro Villagra, and Eduardo M. Sotomayor. "Molecular Pathways in Antigen-Presenting Cells Involved in the Induction of Antigen-specific T-cell Tolerance." In Tumor-Induced Immune Suppression, 411–33. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4899-8056-4_15.

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Izon, David J., John D. Nieland, Lori A. Jones, and Ada M. Kruisbeek. "T Cell Tolerance and Antigen Presenting Cell Function in the Thymus." In Advances in Experimental Medicine and Biology, 159–64. Boston, MA: Springer US, 1993. http://dx.doi.org/10.1007/978-1-4615-2930-9_27.

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Anderton, S. M., C. Burkhart, G. Y. Liu, B. Metzler, and D. C. Wraith. "Antigen-Specific Tolerance Induction and the Immunotherapy of Experimental Autoimmune Disease." In Novartis Foundation Symposia, 120–36. Chichester, UK: John Wiley & Sons, Ltd., 2007. http://dx.doi.org/10.1002/9780470515525.ch9.

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Conference papers on the topic "Antigen tolerance"

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Ruhland, Megan K., Edward W. Roberts, and Matthew F. Krummel. "Abstract B184: Modulating antigen flow to control immune tolerance." In Abstracts: Fourth CRI-CIMT-EATI-AACR International Cancer Immunotherapy Conference: Translating Science into Survival; September 30 - October 3, 2018; New York, NY. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/2326-6074.cricimteatiaacr18-b184.

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Nilsson, I. M., E. Berntorp, and O. Zettervall. "TOLERANCE INDUCTION IN HIGH-RESPONDING HEMOPHILIACS WITH F VIII ANTIBODIES BY MEANS OF COMBINED TREATMENT WITH IgG, CYCLOPHOSPHAMIDE AND F VIII." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644717.

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Of 10 patients with hemophilia A and antibodies, 7 have been rendered tolerant by means of combined treatment with high-dose IgG i.v., cyclophosphamide and F VIII. When the initial antibody concentration exceeded 10 Bethesda inhibitor units per ml, the treatment was preceded by antibody adsorption to protein A. Six of the tolerant patients were originally classified as high-responders. After one week of the combined treatment, VI11:C dropped and the inhibitor reappeared in low titer. The F VIII infusions being continued alone, the inhibitor disappeared in the following week and VIII:C increased satisfactorily after infusion, while VIII:Ag (assayed immunoradiometrically) reached very high concentrations. In one patient the treatment had to be repeated once. Except for transient leukopenia, no side effects occurred. Earlier treatments with F VIII in combination with cyclophosphamide gave high anamnestic response. In two of the remaining three non-tolerant patients, anamnestic response decreased dramatically after two courses of the combined treatment. The tolerant state seems to be stable, as the tolerant patients have now been on regular prophylaxis with F VIII concentrate for periods varying from four months to four years. The half-life of infused F VIII is normal, while that of VIII:Ag is prolonged. On the basis of similar findings in hemophilia B patients, we believe the VIII:Ag to have become modi Tied and complexed to a 'new' antibody which lacks VIII:C inhibitory activity. It is known that modified antigen may act as a tolerogen. The tolerant state may thus be sustained by maintaining consistent concentrations of the modified antigen by means of the F VIII treatment. We conclude that the combined treatment described here is a safe and effective method of tolerance induction in hemophilia A patients.
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Khan, Muhammad Tahir, Toar Imanuel, Yelnil Gabo, and C. W. de Silva. "Robust Multi-Robot Cooperation Using an Idiotypic Model of Artificial Immune Systems." In ASME 2010 International Mechanical Engineering Congress and Exposition. ASMEDC, 2010. http://dx.doi.org/10.1115/imece2010-37966.

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The human immune system is a network of cells, tissues, and other organs that defend the body against foreign invaders called antigens. Jerne’s Idiotypic network theory concerns how an antibody in the immune system stimulates or suppresses another antibody and recognizes an antigen. Based on the principles of the human immune system and Jerne’s idiotypic network theory this paper presents a method for cooperation among robots in a multi-robot system. The developed cooperative multi-robot system is fully autonomous and distributed. In the present paper, cooperation is not assumed a priori. If a robot is unable to complete a task alone, the system autonomously chooses the appropriate number of suitable and most capable robots in the fleet to cooperate with each other in carrying out a global task. The approach developed in the paper incorporates robustness and fault tolerance in immune system–based multi-robot cooperation.
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Nordfang, O., M. Ezban, and J. B. Knudsen. "IMMUNOASSAY FOR FACTOR VIII-HEAVY CHAIN. AN INDICATOR FOR IMMUNE COMPLEXES DURING HIGH DOSE FVIII INHIBITOR TREATMENT." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644718.

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Specificity studies have shown that most hemophilia A inhibitor antibodies are directed towards the light chain of coagulation factor VIII (FVIII). Thus, conventional immunoassays for FVIII-antigen (FVIII:Ag) presumably have reactivity for FVIII-Light Chain (FVIII-LC) . Our sandwich FVIII :Ag assay has been shewn to be specific for only FVIII-LC. We have now developed a specific immunoassay for FVIII-Heavy Chain (FVIII-HC) . This has made it possible to investigate the FVIII-HC content in hemophilia A plasma, and to study the expression of FVIII-HC in culture medium frcm transfected cell lines.By adding purified FVIII-LC and FVIII-HC in coagulation inhibition assay, plasma frcm one of seven hemophilia A inhibitor patients was found to be reactive with both FVIII-LC and FVIII-HC. IgG frcm this plasma was used for a FVIII-HC specific inhibition radioimmunoassay. The polyspecific antibodies were coated to microplates with removable wells. The coated wells were incubated with test sample and with purified 125I-FVIII-HC. When normal human plasma pool contains 1 U/ml of FVIII-HC, the sensitivity of the assay was 0.004 U/ml.For normal plasma and plasma frcm non inhibitor hemophilia A patients, FVIII-HC measurements correlated with FVIII:C and FVIII-LC measurements. However, after FVIII injection hemophilia A inhibitor patients in high dose FVIII treatment showed a much higher FVIII-HC content (1-5 U/ml) than FVIII-LC and FVIII:C (< 0.05 U/ml). These patients have previously been shown to have antibodies towards FVIII-LC. Therefore the antigen measurements indicate that inhibitor patients in high dose FVIII treatment have FVIII/anti-FVIII-LC immune complexes. These circulating immune complexes may be the mediator of an antibody dependent immune tolerance, during the high dose FVIII treatment.
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Ryabov, Vladimir, Peter Pushko, Irina Tretyakova, Rikka Saito, Richard B. Alexander, and Elena N. Klyushnenkova. "Abstract 2880: Novel alphavirus-based vaccine targets dendritic cells and efficiently breaks immunological tolerance to “self” tumor-associated antigen (PSA) in an HLA-DR mouse model of prostate cancer." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-2880.

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Jachetti, Elena, Alice Rigoni, Lucia Bongiovanni, Claudio Tripodo, and Mario P. Colombo. "Abstract 4054: Mast cells contribute to T cell tolerance against prostate cancer- associated antigens favoring tumor growth." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-4054.

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Grasso, C., JS Hähnlein, R. Nadafi, TA De Jong, TH Ramwadhdoebe, JF Semmelink, DM Gerlag, et al. "P113/O17 Human lymph node stromal cells express self-antigens targeted by anti-citrullinated protein antybodies: role for tolerance induction in rheumathoid arthritis." In 39th European Workshop for Rheumatology Research, 28 February–2 March 2019, Lyon, France. BMJ Publishing Group Ltd and European League Against Rheumatism, 2019. http://dx.doi.org/10.1136/annrheumdis-2018-ewrr2019.101.

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Bryson, Paul D., Xiaolu Han, Norman Truong, and Pin Wang. "Abstract 2888: Dendritic cell-targeted lentiviral vector vaccines overcome tolerance to generate a protective T-cell immune response to breast cancer antigens ERBB2 and α-lactalbumin." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-2888.

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Pere, Helene, Yves Montier, Jagadeesh Bayry, Françoise Quintin-Colonna, Nathalie Merillon, Patrice Ravel, Cecile Badoual, et al. "Abstract 752: A CCR4 antagonist combined with protein-or DNA-based vaccines efficiently breaks tolerance and elicits CD8+T cells directed against self and viral associated tumor antigens." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-752.

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