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Books on the topic 'Peripheral t cell tolerance'

Author: Grafiati

Published: 4 June 2021

Last updated: 3 February 2022

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1

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

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2

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

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3

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

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4

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

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5

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

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6

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

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7

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

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8

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

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9

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

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10

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

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11

Dörner, Thomas, and Peter E. Lipsky. Cellular side of acquired immunity (B cells). Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0050.

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B cells have gained interest in rheumatoid arthritis (RA) beyond being the precursors of antibody-producing plasma cells since they are also a broader component of the adaptive immune system. They are capable of functioning as antigen-presenting cells for T-cell activation and can produce an array of cytokines. Disturbances of peripheral B-cell homeostasis together with the formation of ectopic lymphoid neogenesis within the inflamed synovium appears to be a characteristic of patients with RA. Enhanced generation of memory B cells and autoreactive plasma cells producing IgM-RF and ACPA-IgG antibodies together with formation of immune complexes contribute to the maintenance of RA, whereas treatment with B-cell-directed anti-CD20 therapy provides clinical benefit.

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12

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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13

Breban, Maxime, and Hill Gaston. Immune mechanisms: adaptive immunity. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198734444.003.0008.

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The role of adaptive immunity (i.e. the involvement of B and T lymphocytes) in the pathogenesis of axial spondyloarthritis has been investigated in both human disease and relevant animal models. Studies of B cell responses have not generally implicated an autoantibody in the disease, but there are abnormalities of antibody responses, particularly increased titres of antibodies to various gut bacteria. T cells are critical to the disease in animal models other than those where overexpression of a cytokine is engineered, suggesting that they are the drivers of the inflammatory response. There is convergent evidence from animal models, genetics in humans, and direct observation of human peripheral blood and joints to implicate T cells producing IL-17 under the influence of IL-23. These in turn may be responding to bacteria either in the gut or on the skin.

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14

Hartigan-O’Connor, Dennis J., and Christian Brander. Immunology. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190493097.003.0005.

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The key factor in HIV pathogenesis is the decline in CD4+ T cells with resultant immunodeficiency and chronic inflammation. Depletion of CD4+ T cells from the gastrointestinal mucosa followed by microbial translocation and subsequent immune activation are components of disease progression in untreated patients. Symptomatic and occult opportunistic infections including cytomegalovirus contribute to chronic inflammation in persons infected with HIV. Antiretroviral therapy (ART) results in immune reconstitution, with increases in peripheral CD4+ T cell lymphocytes in most persons infected with HIV, although immune recovery is quite variable. A subset of patients with AIDS will develop immune reconstitution inflammatory syndromes after initiation of ART. Approximately 1% of persons with HIV are able to control infection without the need for ART (“elite” controllers). A variety of immune-based therapies, including hydroxyurea, growth hormone, and statins, are being studied in clinical trials and may ultimately play a role in treating persons with HIV infection.

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15

(Editor), T. Kumazawa, L. Kruger (Editor), and K. Mizumura (Editor), eds. The Polymodal Receptor - A Gateway to Pathological Pain (Progress in Brain Research). Elsevier Science, 1996.

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16

Takao, Kumazawa, Kruger Lawrence, and Mizumura Kazue, eds. The polymodal receptor: A gateway to pathological pain. Amsterdam: Elsevier, 1996.

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