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Journal articles on the topic 'Antigen tolerance'

Author: Grafiati

Published: 4 June 2021

Last updated: 11 February 2022

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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 (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 influ

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Carmona, Priscila, Yordanka Medina-Armenteros, Amanda Cabral, et al. "Regulatory/inflammatory cellular response discrimination in operational tolerance." Nephrology Dialysis Transplantation 34, no. 12 (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 heal

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Taylor, Justin J., Ryan J. Martinez, Philip J. Titcombe, et al. "Deletion and anergy of polyclonal B cells specific for ubiquitous membrane-bound self-antigen." Journal of Experimental Medicine 209, no. 11 (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 o

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Chung, Yeonseok, Jae-Hoon Chang, Mi-Na Kweon, Paul D. Rennert та Chang-Yuil Kang. "CD8α–11b+ dendritic cells but not CD8α+ dendritic cells mediate cross-tolerance toward intestinal antigens". Blood 106, № 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

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Duong, Bao Hoa, Hua Tian, Takayuki 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 (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 presen

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Jung, Kyeong Cheon, Chung-Gyu Park, Yoon Kyung Jeon, 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 (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

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Feng, Xiangru, Jiaxue Liu, Weiguo Xu, Gao Li, and Jianxun Ding. "Tackling autoimmunity with nanomedicines." Nanomedicine 15, no. 16 (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 t

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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 (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 h

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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 (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 nonpare

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Parks, Christopher A., Kalli R. Henning, Kevin D. Pavelko, et al. "Breaking tolerance with engineered class I antigen-presenting molecules." Proceedings of the National Academy of Sciences 116, no. 8 (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 influen

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11

Worbs, Tim, Ulrike Bode, Sheng Yan, et al. "Oral tolerance originates in the intestinal immune system and relies on antigen carriage by dendritic cells." Journal of Experimental Medicine 203, no. 3 (2006): 519–27. http://dx.doi.org/10.1084/jem.20052016.

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Oral tolerance induction is a key feature of intestinal immunity, generating systemic nonresponsiveness to ingested antigens. In this study, we report that orally applied soluble antigens are exclusively recognized in the intestinal immune system, particularly in the mesenteric lymph nodes. Consequently, the initiation of oral tolerance is impeded by mesenteric lymphadenectomy. Small bowel transplantation reveals that mesenteric lymph nodes require afferent lymph to accomplish the recognition of orally applied antigens. Finally, oral tolerance cannot be induced in CCR7-deficient mice that disp

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HOYNE, GERARD F, KAREN TAN, MARTA CORSIN-JIMENEZ, et al. "Immunological Tolerance to Inhaled Antigen." American Journal of Respiratory and Critical Care Medicine 162, supplement_3 (2000): S169—S174. http://dx.doi.org/10.1164/ajrccm.162.supplement_3.15tac6.

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13

WEINER, HOWARD L., Z. JENNY ZHANG, SAMIA J. KHOURY, et al. "Antigen-Driven Peripheral Immune Tolerance." Annals of the New York Academy of Sciences 636, no. 1 Antigen and C (1991): 227–32. http://dx.doi.org/10.1111/j.1749-6632.1991.tb33454.x.

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14

Kontos, Stephan, Alizée J. Grimm, and Jeffrey A. Hubbell. "Engineering antigen-specific immunological tolerance." Current Opinion in Immunology 35 (August 2015): 80–88. http://dx.doi.org/10.1016/j.coi.2015.05.005.

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15

Ferry, Helen, Margaret Jones, David J. Vaux, Ian S. D. Roberts, and Richard J. Cornall. "The Cellular Location of Self-antigen Determines the Positive and Negative Selection of Autoreactive B Cells." Journal of Experimental Medicine 198, no. 9 (2003): 1415–25. http://dx.doi.org/10.1084/jem.20030279.

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Systemic autoimmune disease is frequently characterized by the production of autoantibodies against widely expressed intracellular self-antigens, whereas B cell tolerance to ubiquitous and highly expressed extracellular antigens is strictly enforced. To test for differences in the B cell response to intracellular and extracellular self-antigens, we sequestered a tolerogenic cell surface antigen intracellularly by addition of a two amino acid endoplasmic reticulum (ER) retention signal. In contrast to cell surface antigen, which causes the deletion of autoreactive B cells, the intracellularly s

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16

Avichezer, Dody, Rafael S. Grajewski, Chi-Chao Chan, et al. "An Immunologically Privileged Retinal Antigen Elicits Tolerance." Journal of Experimental Medicine 198, no. 11 (2003): 1665–76. http://dx.doi.org/10.1084/jem.20030413.

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Immunologically privileged retinal antigens can serve as targets of experimental autoimmune uveitis (EAU), a model for human uveitis. The tolerance status of susceptible strains, whose target antigen is not expressed in the thymus at detectable levels, is unclear. Here, we address this issue directly by analyzing the consequences of genetic deficiency versus sufficiency of a uveitogenic retinal antigen, interphotoreceptor retinoid-binding protein (IRBP). IRBP-knockout (KO) and wild-type (WT) mice on a highly EAU-susceptible background were challenged with IRBP. The KO mice had greatly elevated

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17

Li, Xuemei, and Xiaoxia Li. "Progress of research on the immune tolerance of chronic HBV infection." Infection International 7, no. 3 (2018): 88–93. http://dx.doi.org/10.2478/ii-2018-0026.

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Abstract Immune tolerance is a specific lack or negative response of T and B lymphocytes to antigen. According to different formation periods, immune tolerance can be divided into central and peripheral tolerances. The immune tolerance of the body to hepatitis B virus (HBV) after infection is the main cause of chronic HBV infection. In this paper, the functional defects of hepatitis B virus e antigen and dendritic cells, hyporesponsiveness of cytotoxic T lymphocyte, variation of helper T lymphocytes and cytokines, HBV genotype and genome, and the role of host gene polymorphism in the formation

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18

Maldonado, Roberto A., Robert A. LaMothe, Joseph D. Ferrari, et al. "Polymeric synthetic nanoparticles for the induction of antigen-specific immunological tolerance." Proceedings of the National Academy of Sciences 112, no. 2 (2014): E156—E165. http://dx.doi.org/10.1073/pnas.1408686111.

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Current treatments to control pathological or unwanted immune responses often use broadly immunosuppressive drugs. New approaches to induce antigen-specific immunological tolerance that control both cellular and humoral immune responses are desirable. Here we describe the use of synthetic, biodegradable nanoparticles carrying either protein or peptide antigens and a tolerogenic immunomodulator, rapamycin, to induce durable and antigen-specific immune tolerance, even in the presence of potent Toll-like receptor agonists. Treatment with tolerogenic nanoparticles results in the inhibition of CD4+

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19

Smith, Nicole H., Eldad A. Hod, Steven L. Spitalnik, James C. Zimring, and Jeanne E. Hendrickson. "Transfusion in the absence of inflammation induces antigen-specific tolerance to murine RBCs." Blood 119, no. 6 (2012): 1566–69. http://dx.doi.org/10.1182/blood-2011-09-382655.

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Abstract Most human transfusion recipients fail to make detectable alloantibodies to foreign RBC antigens (“nonresponders”). Herein, we use a murine model to test the hypothesis that nonresponders may be immunologically tolerant. FVB mice transfused with RBCs expressing transgenic human glycophorin A (hGPA) antigen in the absence of inflammation produced undetectable levels of anti-hGPA immunoglobulins, unlike those transfused in the presence of polyinosinic:polycytidylic acid–induced inflammation. Mice in the nonresponder group failed to produce anti-hGPA after subsequent transfusions in the

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Robert, S., K. Van Huynegem, C. Gysemans, C. Mathieu, P. Rottiers, and L. Steidler. "Trimming of two major type 1 diabetes driving antigens, GAD65 and IA-2, allows for successful expression in Lactococcus lactis." Beneficial Microbes 6, no. 4 (2015): 591–601. http://dx.doi.org/10.3920/bm2014.0083.

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Type 1 diabetes (T1D) is a chronic autoimmune disease characterised by excessive immune reactions against auto-antigens of pancreatic β-cells. Restoring auto-antigen tolerance remains the superior therapeutic strategy. Oral auto-antigen administration uses the tolerogenic nature of the gut-associated immune system to induce antigen-specific tolerance. However, due to gastric degradation, proper mucosal product delivery often imposes a challenge. Recombinant Lactococcus lactis have proven to be effective and safe carriers for gastrointestinal delivery of therapeutic products: L. lactis secretin

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21

Shrestha, Umid Kumar. "Immunology of the gut and oral tolerance." Journal of Advances in Internal Medicine 4, no. 1 (2015): 16–24. http://dx.doi.org/10.3126/jaim.v4i1.14176.

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The pathogens and harmless antigens from the bacterial flora and food constantly expose the mucosal surface of the gastrointestinal tract. The mucosal epithelial cells act not only as a physical barrier, but also as a local immune system, which plays a vital role in defense and self-tolerance. The gut mucosal immune system comprises several compartments: Peyer’s patches and lymphoid follicles in the colonic mucosa, and lymphocytes in the lamina propria and intraepithelial lymphocytes. Peyer’s patches mediate antigen uptake via specialized epithelial cells (M cells) and are rich in B cells for

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Belz, Gabrielle T., Georg M. N. Behrens, Chris M. Smith та ін. "The CD8α+ Dendritic Cell Is Responsible for Inducing Peripheral Self-Tolerance to Tissue-associated Antigens". Journal of Experimental Medicine 196, № 8 (2002): 1099–104. http://dx.doi.org/10.1084/jem.20020861.

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We previously described a mechanism for the maintenance of peripheral self-tolerance. This involves the cross-presentation of tissue-associated antigens by a bone marrow–derived cell type that stimulates the proliferation and ultimate deletion of self-reactive CD8 T cells. This process has been referred to as cross-tolerance. Here, we characterize the elusive cell type responsible for inducing cross-tolerance as a CD8α+ dendritic cell (DC). To achieve this aim, transgenic mice were generated expressing yellow fluorescent protein (YFP) linked to CTL epitopes for ovalbumin and glycoprotein B (gB

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Doyle, Hester A., Jing Zhou, Martin J. Wolff, et al. "Isoaspartyl Post-translational Modification Triggers Anti-tumor T and B Lymphocyte Immunity." Journal of Biological Chemistry 281, no. 43 (2006): 32676–83. http://dx.doi.org/10.1074/jbc.m604847200.

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A hallmark of the immune system is the ability to ignore self-antigens. In attempts to bypass normal immune tolerance, a post-translational protein modification was introduced into self-antigens to break T and B cell tolerance. We demonstrate that immune tolerance is bypassed by immunization with a post-translationally modified melanoma antigen. In particular, the conversion of an aspartic acid to an isoaspartic acid within the melanoma antigen tyrosinase-related protein (TRP)-2 peptide-(181-188) makes the otherwise immunologically ignored TRP-2 antigen immunogenic. Tetramer analysis of iso-As

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Eynon, E. E., and D. C. Parker. "Small B cells as antigen-presenting cells in the induction of tolerance to soluble protein antigens." Journal of Experimental Medicine 175, no. 1 (1992): 131–38. http://dx.doi.org/10.1084/jem.175.1.131.

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We have investigated the ability of resting B cells, acting as antigen-presenting cells, to induce tolerance to soluble protein antigens in mice, using an antigen targeted specifically to B cells. We inject mice intravenously with ultracentrifuged Fab fragments of rabbit anti-mouse immunoglobulin D (IgD) (Fab anti-delta). Treatment with Fab anti-delta results in profound tolerance to challenge with 100 micrograms Fab nonimmune rabbit Ig (Fab NRG), precipitated in alum, as measured by antibody production. Tolerance to rabbit Fab is antigen specific, since the treated mice make normal antibody r

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Fukaya, Tomohiro, Hideaki Takagi, Yumiko Sato, et al. "Crucial roles of B7-H1 and B7-DC expressed on mesenteric lymph node dendritic cells in the generation of antigen-specific CD4+Foxp3+ regulatory T cells in the establishment of oral tolerance." Blood 116, no. 13 (2010): 2266–76. http://dx.doi.org/10.1182/blood-2009-10-250472.

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Abstract Oral tolerance is a key feature of intestinal immunity, generating systemic tolerance to fed antigens. However, the molecular mechanism mediating oral tolerance remains unclear. In this study, we examined the role of the B7 family members of costimulatory molecules in the establishment of oral tolerance. Deficiencies of B7-H1 and B7-DC abrogated the oral tolerance, accompanied by enhanced antigen-specific CD4+ T-cell response and IgG1 production. Mesenteric lymph node (MLN) dendritic cells (DCs) displayed higher levels of B7-H1 and B7-DC than systemic DCs, whereas they showed similar

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Adler, Adam J., David W. Marsh, Gregory S. Yochum, et al. "CD4+ T Cell Tolerance to Parenchymal Self-Antigens Requires Presentation by Bone Marrow–derived Antigen-presenting Cells." Journal of Experimental Medicine 187, no. 10 (1998): 1555–64. http://dx.doi.org/10.1084/jem.187.10.1555.

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T cell tolerance to parenchymal self-antigens is thought to be induced by encounter of the T cell with its cognate peptide–major histocompatibility complex (MHC) ligand expressed on the parenchymal cell, which lacks appropriate costimulatory function. We have used a model system in which naive T cell receptor (TCR) transgenic hemagglutinin (HA)-specific CD4+ T cells are adoptively transferred into mice expressing HA as a self-antigen on parenchymal cells. After transfer, HA-specific T cells develop a phenotype indicative of TCR engagement and are rendered functionally tolerant. However, T cell

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Von Bubnoff, D., H. De La Salle, J. Weßendorf, S. Koch, D. Hanau, and T. Bieber. "Antigen-presenting cells and tolerance induction." Allergy 57, no. 1 (2002): 2–8. http://dx.doi.org/10.1046/j.0105-4538.2001.00001.x-i4.

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Parker, David C., and Elizabeth E. Eynon. "Antigen presentation in acquired immunological tolerance." FASEB Journal 5, no. 13 (1991): 2777–84. http://dx.doi.org/10.1096/fasebj.5.13.1916102.

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von Bubnoff, D., H. de la Salle, J. Wessendorf, S. Koch, D. Hanau, and T. Bieber. "Antigen-presenting cells and tolerance induction." Allergy 57, no. 1 (2002): 2–8. http://dx.doi.org/10.1034/j.1398-9995.2002.01150.x.

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&NA;. "DELETIONAL TOLERANCE TO A MODEL ANTIGEN." Transplantation 82, Suppl 2 (2006): 893. http://dx.doi.org/10.1097/00007890-200607152-02500.

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MORRIS, PETER J., KATHRYN J. WOOD, and MARGARET J. DALLMAN. "Antigen-Induced Tolerance to Organ Allografts." Annals of the New York Academy of Sciences 636, no. 1 Antigen and C (1991): 295–305. http://dx.doi.org/10.1111/j.1749-6632.1991.tb33460.x.

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Öhlén, Claes, Michael Kalos, Laurence E. Cheng, et al. "CD8+ T Cell Tolerance to a Tumor-associated Antigen Is Maintained at the Level of Expansion Rather than Effector Function." Journal of Experimental Medicine 195, no. 11 (2002): 1407–18. http://dx.doi.org/10.1084/jem.20011063.

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CD8+ T cell tolerance to self-proteins prevents autoimmunity but represents an obstacle to generating T cell responses to tumor-associated antigens. We have made a T cell receptor (TCR) transgenic mouse specific for a tumor antigen and crossed TCR-TG mice to transgenic mice expressing the tumor antigen in hepatocytes (gag-TG). TCRxgag mice showed no signs of autoimmunity despite persistence of high avidity transgenic CD8+ T cells in the periphery. Peripheral CD8+ T cells expressed phenotypic markers consistent with antigen encounter in vivo and had upregulated the antiapoptotic molecule Bcl-2.

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Krishnan, Lakshmi, Lise Deschatelets, Felicity C. Stark, Komal Gurnani, and G. Dennis Sprott. "Archaeosome Adjuvant Overcomes Tolerance to Tumor-Associated Melanoma Antigens Inducing Protective CD8+T Cell Responses." Clinical and Developmental Immunology 2010 (2010): 1–13. http://dx.doi.org/10.1155/2010/578432.

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Vesicles comprised of the ether glycerolipids of the archaeonMethanobrevibacter smithii(archaeosomes) are potent adjuvants for evoking CD8+T cell responses. We therefore explored the ability of archaeosomes to overcome immunologic tolerance to self-antigens. Priming and boosting of mice with archaeosome-antigen evoked comparable CD8+T cell response and tumor protection to an alternate boosting strategy utilizing live bacterial vectors for antigen delivery. Vaccination with melanoma antigenic peptides TRP181-189and Gp10025-33delivered in archaeosomes resulted in IFN-γproducing antigen-specific

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Ogawa, Haruko, Deng-Ping Yin, Jikun Shen, and Uri Galili. "Tolerance induction to a mammalian blood group–like carbohydrate antigen by syngeneic lymphocytes expressing the antigen." Blood 101, no. 6 (2003): 2318–20. http://dx.doi.org/10.1182/blood-2002-07-2151.

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Tolerance induction to transplantation-associated carbohydrate antigens, such as blood group A or B and the α-gal epitope (Galα1-3Galβ1-4GlcNAc-R), is of clinical significance. This study demonstrates tolerance induction to the α-gal epitope in the experimental animal model of α1,3galactosyltransferanse knockout mice (KO mice) lacking α-gal epitopes by administering syngeneic lymphocytes expressing α-gal epitopes. Repeated immunization of control KO mice with pig kidney membranes (PKM) expressing many α-gal epitopes induces an extensive anti-Gal antibody response against this epitope. In contr

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Wang, Hongwei, Fengdong Cheng, Alex Cuenca, et al. "Imatinib mesylate (STI-571) enhances antigen-presenting cell function and overcomes tumor-induced CD4+ T-cell tolerance." Blood 105, no. 3 (2005): 1135–43. http://dx.doi.org/10.1182/blood-2004-01-0027.

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Abstract Tumor antigen–specific T-cell tolerance imposes a significant barrier to the development of effective therapeutic cancer vaccines. Bone marrow–derived antigen-presenting cells (APCs) are critical in the induction of this unresponsive state. Here we show that in vitro treatment of APCs with the tyrosine kinase inhibitor, imatinib mesylate (STI-571), enhances the activation of naive antigen-specific T cells and restores the responsiveness of tolerant T cells from tumor-bearing hosts. Furthermore, in vivo treatment with STI-571 not only prevented the induction of tolerance in tumor-speci

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Chung, Chun Yuen J., Dirk Ysebaert, Zwi N. Berneman, and Nathalie Cools. "Dendritic Cells: Cellular Mediators for Immunological Tolerance." Clinical and Developmental Immunology 2013 (2013): 1–8. http://dx.doi.org/10.1155/2013/972865.

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In general, immunological tolerance is acquired upon treatment with non-specific immunosuppressive drugs. This indiscriminate immunosuppression of the patient often causes serious side-effects, such as opportunistic infectious diseases. Therefore, the need for antigen-specific modulation of pathogenic immune responses is of crucial importance in the treatment of inflammatory diseases. In this perspective, dendritic cells (DCs) can have an important immune-regulatory function, besides their notorious antigen-presenting capacity. DCs appear to be essential for both central and peripheral toleran

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Perdicchio, Maurizio, Juan M. Ilarregui, Marleen I. Verstege, et al. "Sialic acid-modified antigens impose tolerance via inhibition of T-cell proliferation and de novo induction of regulatory T cells." Proceedings of the National Academy of Sciences 113, no. 12 (2016): 3329–34. http://dx.doi.org/10.1073/pnas.1507706113.

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Sialic acids are negatively charged nine-carbon carboxylated monosaccharides that often cap glycans on glycosylated proteins and lipids. Because of their strategic location at the cell surface, sialic acids contribute to interactions that are critical for immune homeostasis via interactions with sialic acid-binding Ig-type lectins (siglecs). In particular, these interactions may be of importance in cases where sialic acids may be overexpressed, such as on certain pathogens and tumors. We now demonstrate that modification of antigens with sialic acids (Sia-antigens) regulates the generation of

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Sotomayor, Eduardo M., Ivan Borrello, Frédérique-Marie Rattis, et al. "Cross-presentation of tumor antigens by bone marrow–derived antigen-presenting cells is the dominant mechanism in the induction of T-cell tolerance during B-cell lymphoma progression." Blood 98, no. 4 (2001): 1070–77. http://dx.doi.org/10.1182/blood.v98.4.1070.

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Tumor antigen-specific T-cell tolerance may limit the efficacy of therapeutic cancer vaccines. Direct presentation of antigens by tumor cells incapable of providing adequate costimulation to tumor-specific T cells has been suggested as the basis for this unresponsiveness. Using parent-into-F1 bone marrow (BM) chimeras, this study unambiguously demonstrates that the induction of this tolerant state requires T-cell recognition of tumor antigen presented by BM-derived antigen-presenting cells (APCs), not tumor cells themselves. In the absence of host APC presentation, tumor-specific T cells remai

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Peschl, Patrick, Markus Reindl, Kathrin Schanda, Mireia Sospedra, Roland Martin, and Andreas Lutterotti. "Antibody responses following induction of antigen-specific tolerance with antigen-coupled cells." Multiple Sclerosis Journal 21, no. 5 (2014): 651–55. http://dx.doi.org/10.1177/1352458514549405.

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We have recently demonstrated the safety and tolerability of a novel therapeutic regimen employing autologous blood cells chemically coupled with seven myelin peptides to induce antigen-specific tolerance in MS (ETIMS study). The aim of the current study was an extended safety analysis to assess the effect of the ETIMS approach on antibodies to common autoantigens, the myelin peptides used and common recall antigens. None of the patients showed induction of autoantibody responses. One patient had a measurable myelin peptide-specific response at baseline, which was reduced after treatment. Tota

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Bam, Marpe, and Tamishraha Bagchi. "MART-1 transcript is absent in PBMCs from Vitiligo patients." Open Life Sciences 4, no. 4 (2009): 528–35. http://dx.doi.org/10.2478/s11535-009-0057-6.

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AbstractMechanisms occurring in the thymus and periphery are responsible for the generation and maintenance of tolerance in the immune system. Various reports have shown that the existence of an antigen in the peripheral circulation results in tolerance induction towards that protein. These observations imply that the lack of a self antigen can lead to induction of autoimmunity. Previously we have reported that Tyrosinase related protein-2 (TRP-2) transcripts from peripheral blood mononuclear cells (PBMCs) are absent in vitiligo patients but present in healthy individuals. Here, we show that M

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Wilcox, Ryan A., Koji Tamada, Dallas B. Flies, et al. "Ligation of CD137 receptor prevents and reverses established anergy of CD8+ cytolytic T lymphocytes in vivo." Blood 103, no. 1 (2004): 177–84. http://dx.doi.org/10.1182/blood-2003-06-2184.

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Abstract T-cell anergy is a tolerance mechanism defined as a hyporesponsive status of antigen-specific T cells upon prior antigen encounter and is believed to play a critical role in the evasion of tumor immunity and the amelioration of allogeneic transplant rejection. Molecular mechanisms in controlling T-cell anergy are less known. We show here that administration of an agonistic monoclonal antibody (mAb) to CD137, a member of the tumor necrosis factor receptor superfamily, prevents the induction of CD8+ cytolytic T-lymphocyte (CTL) anergy by soluble antigens. More importantly, CD137 mAb res

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Ghorashian, Sara, Ben Carpenter, Angelika Holler, et al. "CD4 Cells Engineered to Express an MHC Class I Restricted TCR Can Rescue CD8 Cells Tolerized to Tumour-Associated Antigens." Blood 120, no. 21 (2012): 952. http://dx.doi.org/10.1182/blood.v120.21.952.952.

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Abstract Abstract 952 Background: The efficacy of T cell therapies for cancer may be limited when targeting tumour-associated antigens (TAA) which are also self-antigens. Ongoing exposure to TAA on normal cells may lead to tolerance via anergy or exhaustion of antigen-specific T cells. Methods: We have designed a model of tolerance to TAA in which T cell receptor (TCR)-transduced CD8 T cells recognise pMDM2, a TAA that is also a ubiquitous self-antigen. CD8+ T cells were transduced with pMDM2-specific TCR (MDM-CD8) and transferred to sub-lethally irradiated B6 mice that express pMDM2 in the co

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Morlacchi, Sara, Cristiana Soldani, Antonella Viola, and Adelaida Sarukhan. "Self-antigen presentation by mouse B cells results in regulatory T-cell induction rather than anergy or clonal deletion." Blood 118, no. 4 (2011): 984–91. http://dx.doi.org/10.1182/blood-2011-02-336115.

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Abstract Multiple mechanisms operate to ensure T-cell tolerance toward self-antigens. Three main processes have been described: clonal deletion, anergy, and deviation to CD4+ regulatory T cells (Tregs) that suppress autoreactive T cells that have escaped the first 2 mechanisms. Although it is accepted that dendritic cells (DCs) and B cells contribute in maintaining T-cell tolerance to self-antigens, their relative contribution and the processes involved under physiologic conditions remain only partially characterized. In this study, we used different transgenic mouse models to obtain chimeras

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Soroosh, Pejman, Taylor A. Doherty, Wei Duan, et al. "Lung-resident tissue macrophages generate Foxp3+ regulatory T cells and promote airway tolerance." Journal of Experimental Medicine 210, no. 4 (2013): 775–88. http://dx.doi.org/10.1084/jem.20121849.

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Airway tolerance is the usual outcome of inhalation of harmless antigens. Although T cell deletion and anergy are likely components of tolerogenic mechanisms in the lung, increasing evidence indicates that antigen-specific regulatory T cells (inducible Treg cells [iTreg cells]) that express Foxp3 are also critical. Several lung antigen-presenting cells have been suggested to contribute to tolerance, including alveolar macrophages (MØs), classical dendritic cells (DCs), and plasmacytoid DCs, but whether these possess the attributes required to directly promote the development of Foxp3+ iTreg ce

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Esprit, Arthur, Wout de Mey, Rajendra Bahadur Shahi, Kris Thielemans, Lorenzo Franceschini, and Karine Breckpot. "Neo-Antigen mRNA Vaccines." Vaccines 8, no. 4 (2020): 776. http://dx.doi.org/10.3390/vaccines8040776.

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The interest in therapeutic cancer vaccines has caught enormous attention in recent years due to several breakthroughs in cancer research, among which the finding that successful checkpoint blockade treatments reinvigorate neo-antigen-specific T cells and that successful adoptive cell therapies are directed towards neo-antigens. Neo-antigens are cancer-specific antigens, which develop from somatic mutations in the cancer cell genome that can be highly immunogenic and are not subjected to central tolerance. As the majority of neo-antigens are unique to each patient’s cancer, a vaccine technolog

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Gallegos, Alena M., and Michael J. Bevan. "Central Tolerance to Tissue-specific Antigens Mediated by Direct and Indirect Antigen Presentation." Journal of Experimental Medicine 200, no. 8 (2004): 1039–49. http://dx.doi.org/10.1084/jem.20041457.

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Intrathymic expression of tissue-specific antigens (TSAs) by medullary thymic epithelial cells (Mtecs) leads to deletion of autoreactive T cells. However, because Mtecs are known to be poor antigen-presenting cells (APCs) for tolerance to ubiquitous antigens, and very few Mtecs express a given TSA, it was unclear if central tolerance to TSA was induced directly by Mtec antigen presentation or indirectly by thymic bone marrow (BM)-derived cells via cross-presentation. We show that professional BM-derived APCs acquire TSAs from Mtecs and delete autoreactive CD8 and CD4 T cells. Although direct a

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Cheng, Fengdong, Hongwei Wang, Alex G. Cuenca, et al. "Disruption of STAT3 Signaling in Antigen Presenting Cells Represents a Novel Strategy To Overcome Tumor-Induced Antigen-Specific CD4+ T-Cell Tolerance." Blood 104, no. 11 (2004): 109. http://dx.doi.org/10.1182/blood.v104.11.109.109.

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Abstract Tumor antigen-specific T-cell tolerance imposes a significant barrier to the development of effective therapeutic cancer vaccines. Bone marrow-derived antigen presenting cells (APCs) are critical in the induction of this unresponsive state. Recently, we have identified STAT3 signaling in APCs as an important regulatory pathway that determines the functional outcome of antigen-specific CD4+ T-cells in response to cognate antigen. Indeed, while disruption of this signaling pathway in APCs led to effective T cell priming, enhanced STAT3 activity resulted in the induction of T cell unresp

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Sebille, Fabien, Bernard Vanhove, and Jean-Paul Soulillou. "Mechanisms of tolerance induction: blockade of co–stimulation." Philosophical Transactions of the Royal Society of London. Series B: Biological Sciences 356, no. 1409 (2001): 649–57. http://dx.doi.org/10.1098/rstb.2001.0842.

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Induction of tolerance to transplantation antigens is believed to be a promising way to achieve long–term allograft survival without a deleterious immunosuppressive regimen. T–cell activation, which is an essential feature of graft rejection, requires a first signal provided by T–cell receptor (TCR) ligation and a second signal provided by engagement of co–stimulatory molecules with their respective ligands on antigen–presenting cells. The coordinated triggering of these two independent signalling systems ensures the full T–cell activation, including proliferation and acquisition of effector f

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Menne, Stephan, Carol A. Roneker, Brent E. Korba, John L. Gerin, Bud C. Tennant та Paul J. Cote. "Immunization with Surface Antigen Vaccine Alone and after Treatment with 1-(2-Fluoro-5-Methyl-β-l-Arabinofuranosyl)-Uracil (l-FMAU) Breaks Humoral and Cell-Mediated Immune Tolerance in Chronic Woodchuck Hepatitis Virus Infection". Journal of Virology 76, № 11 (2002): 5305–14. http://dx.doi.org/10.1128/jvi.76.11.5305-5314.2002.

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ABSTRACT Woodchucks chronically infected with the woodchuck hepatitis virus (WHV) were treated with the antiviral drug 1-(2-fluoro-5-methyl-β-l-arabinofuranosyl)-uracil (l-FMAU) or placebo for 32 weeks. Half the woodchucks in each group then received four injections of surface antigen vaccine during the next 16 weeks. Vaccination alone elicited a low-level antibody response to surface antigen in most carriers but did not affect serum WHV DNA and surface antigen. Carriers treated first with l-FMAU to reduce serum WHV DNA and surface antigen and then vaccinated had a similar low-level antibody r

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Kuiper, Johan, and Saskia de Jager. "Vaccination strategies in atherosclerosis." Thrombosis and Haemostasis 106, no. 11 (2011): 796–803. http://dx.doi.org/10.1160/th11-05-0369.

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SummaryThe treatment of atherosclerosis is currently based on lipid lowering in combination with anti-inflammatory therapies that slow the progression of atherosclerosis. Still, we are not able to fully inhibit the formation or progression of atherosclerotic lesions. A very effective strategy in other disease pathologies is vaccination, in which the body is challenged with the culprit protein or micro-organism in order to create a highly specific humoral immune-response. Immunisation can typically be divided into active or passive immunisation. Active immunisation occurs naturally when the bod

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