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Books on the topic 'Antigen tolerance'

Author: Grafiati

Published: 4 June 2021

Last updated: 11 February 2022

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1

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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2

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

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3

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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5

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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6

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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7

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

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8

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

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9

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

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10

(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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11

Morris, Peter J., and Jeremy R. Chapman. The evolution of kidney transplantation. Edited by Jeremy R. Chapman. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0275.

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The history of kidney transplantation starts in 1902 with Ullman transplanting kidneys between dogs, and Carrel’s development of vascular anastomotic techniques. The developments in the 1950s in Boston, Paris, and the laboratories of Medawar and others demonstrated both proof of the principle and some of the barriers to clinical kidney transplantation. The 1960s laid the groundwork for organ preservation, immunosuppression, and histocompatibility leading to the creation of transplant units in many countries. In the 1970s, there was steady progress in understanding the immunology of allograft rejection and its suppression. The advent of azathioprine used with steroids in the early 1960s resulted in 1-year graft survival rates of around 60% and patient survival of 90% in good units. However, with the introduction of ciclosporin in the early 1980s, renal transplantation became an even more reliable renal replacement option as there was a dramatic reduction in the incidence of irreversible acute rejection. The 1990s saw the introduction of both better immunosuppression and better infection prophylaxis, which further improved patient outcomes. The first decade of the twenty-first century has been characterized by the promise of new technologies in many areas, only some of which have delivered clinical benefit. Molecular human leucocyte antigen (HLA) typing and detection of antibodies to HLA antigens, standardized immunosuppression and anti-infective prophylaxis, surveillance biopsy, and developing systems for increasing donation rates are delivering major benefits. Gene biomarkers, stem cell therapy, and tolerance protocols have yet to make an impact. This chapter describes the historical development of transplantation and how it has yielded the results delivered in clinical practice today.

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12

Keshav, Satish, and Alexandra Kent. Immunology and genetics in gastrointestinal and hepatic medicine. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0196.

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The gut has a pivotal role in immune homeostasis. It is constantly exposed to a wide array of antigens in food, and resident and consumed microorganisms. It is estimated that the number of bacterial cells in the gastrointestinal tract is tenfold greater than the number of cells in the human body. The gut needs to recognize harmful bacteria, and consequently contains the largest number of immune cells in the body. However, it must remain tolerant to commensal bacteria. Bacteria express antigens that stimulate an immunological response via the gut-associated lymphoid tissue (GALT). The GALT includes the appendix, tonsils, Peyer’s patches, and mesenteric lymph nodes. Therefore, the intestinal immune system is finely balanced between tolerance and reactivity. An example of an abnormal response that generally the individual should be tolerant to is gliadin peptides in coeliac disease. An example of excessive tolerance to an otherwise controllable infection is cryptosporidiosis, which causes diarrhoea in patients with HIV infection. The understanding of genetics in disease has progressed rapidly with the introduction of genome-wide association studies. The Welcome Trust Case Control Consortium has performed extensive research on the genetics of many illnesses, including Crohn’s disease, ulcerative colitis, Barrett’s oesophagus, oesophageal adenocarcinoma, and primary biliary cholangitis. Although these studies have increased our understanding of the molecular basis of disease, they have had little impact on clinical management. This may change as studies associate genotype and phenotype. Several gastrointestinal diseases have an etiology based on immunological or genetic aberrations, and these immunological mechanisms and genetic mutations can be utilized for diagnostic purposes. However, there is no genetic or immunological marker that is 100% specific to a disease and, consequently, the markers are used to support clinical, histological, and/or radiological findings.

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13

Rogler, Gerhard. Gastrointestinal system. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0021.

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Rheumatic diseases and diseases of the gastrointestinal (GI) tract are connected in two ways. The extraintestinal manifestations of inflammatory GI diseases such as inflammatory bowel disease affect joints in up to one-third of patients. On the other hand, several rheumatic diseases such as vasculitis or systemic lupus erythematosus (SLE) induce a wide spectrum of gastrointestinal manifestations. The GI tract constitutes a huge area in contact with the environment. It is exposed to billions of food antigens, commensal bacteria, and potential pathogens. Some of those antigens are thought to play a role in the pathogenesis of rheumatic diseases. The intestinal barrier function and the gut immune system are tightly regulated, as on one hand tolerance for food antigens and the resident commensal flora needs to be maintained, and on the other hand pathogens need to be rapidly and effectively eliminated. Non-infectious, chronic inflammatory diseases of the small and large intestine with rheumatic manifestations have been well known for decades. Among the susceptibility genes for Crohn's disease and ulcerative colitis are some that also cause susceptibility to rheumatoid arthritis or SLE, indicating a shared susceptibility and overlapping pathological mechanisms. Subsequently, similar therapeutic principles have successfully been applied in autoimmune GI and rheumatological diseases such as steroids, immunosuppressants, and anti-TNF (tumour necrosis factor) antibodies.

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14

Muthukumar, Thangamani, Darshana Dadhania, Choli Hartono, and Manikkam Suthanthiran. Immunology, sensitization, and histocompatibility. Edited by Jeremy R. Chapman. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0279.

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Allograft rejection of the histo-incompatible allograft involves a highly orchestrated action of multiple cell types and mediators, with lymphocytes responsible for the identification of the foreignness of the allograft. The immune response directed against the donor is primarily, but not exclusively, directed at the donor’s major histocompatibility complex region class I and class II proteins. This chapter describes the immunobiology of the T cell and the role of human leucocyte antigens in clinical transplantation, thus identifying the targets for manipulation of the immune response by immune suppressants and through strategies designed to create a state of tolerance of the allograft.

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15

Afzali, Behdad, and Claudia Kemper. Immunity. Edited by David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0128.

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Immunological health relies on a balance between immune responsiveness to foreign pathogens and tolerance to self-components, commensals, food-derived components, and semi-allogeneic fetal antigens. Disruptions of this balance are hallmarks of immunodeficiency diseases, autoimmune diseases, and pregnancy failure. Patients with chronic kidney disease are immunologically unique in demonstrating features of both chronic inflammation and acquired immunodeficiency—predisposing these individuals to the two commonest causes of death, namely cardiovascular disease and sepsis. Defects and abnormalities in almost all components of the immune system can be observed, although it is difficult to say whether the observations denote mechanism or effect. This chapter reviews, briefly, measurable immune system abnormalities in chronic kidney disease and some of the potential underlying mechanisms.

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16

O'Dwyer, Conor. Coming Out of Communism. NYU Press, 2018. http://dx.doi.org/10.18574/nyu/9781479876631.001.0001.

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This book offers a close study of the rapidly evolving politics of LGBT rights in postcommunist Europe, where social attitudes have historically marginalized the issue and where the legacy of weak civil society has handicapped activism in general. What happens in societies such as these when increased exposure to transnational institutions such as the European Union and the minority-rights norms that they promote brings new visibility to LGBT issues? Is activism boosted by the infusion of resources from transnational networks? Or does transnational pressure bring backlash, inflaming antigay attitudes and driving activism underground? This study uncovers and explains the surprising divergence in the organization of LGBT activism in postcommunist Europe, focusing on Poland and the Czech Republic from the late 1980s through 2012. Hungary, Slovakia, and Romania form additional case studies. It argues that domestic backlash against transnational rights norms has been a primary catalyst for organizational development in the region’s most robust LGBT movements. It offers a comparative framework of broader relevance describing the conditions under which transnational pressure and domestic politics may interact to build robust activism, or not. This theorization offers resolution for a striking puzzle of LGBT politics in the countries examined: Why is the most organized and influential activism often found in societies where attitudes toward homosexuality are least tolerant? The book uses a multimethod research design drawing on field interviews, original sources, and participant observation to process trace how the framing of homosexuality and the organization of LGBT activism change in historical time.

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