Autoimmune diseases in the TH17 era

Autoimmune diseases in the TH17 era

Author Mesquita Júnior, Danilo Autor UNIFESP Google Scholar
Cruvinel, Wilson de Melo Autor UNIFESP Google Scholar
Câmara, Niels Olsen Saraiva Autor UNIFESP Google Scholar
Kállas, E.g. Google Scholar
Andrade, Luiz Eduardo Coelho Autor UNIFESP Google Scholar
Institution Universidade Federal de São Paulo (UNIFESP)
Universidade de São Paulo (USP)
Universidade Católica de Goiás Departamento de Biomedicina
Abstract A new subtype of CD4+ T lymphocytes characterized by the production of interleukin 17, i.e., TH17 cells, has been recently described. This novel T cell subset is distinct from type 1 and type 2 T helper cells. The major feature of this subpopulation is to generate significant amounts of pro-inflammatory cytokines, therefore appearing to be critically involved in protection against infection caused by extracellular microorganisms, and in the pathogenesis of autoimmune diseases and allergy. The dynamic balance among subsets of T cells is important for the modulation of several steps of the immune response. Disturbances in this balance may cause a shift from normal immunologic physiology to the development of immune-mediated disorders. In autoimmune diseases, the fine balance between the proportion and degree of activation of the various T lymphocyte subsets can contribute to persistent undesirable inflammatory responses and tissue replacement by fibrosis. This review highlights the importance of TH17 cells in this process by providing an update on the biology of these cells and focusing on their biology and differentiation processes in the context of immune-mediated chronic inflammatory diseases.
Keywords Autoimmune diseases
TH17 cells
Language English
Date 2009-06-01
Published in Brazilian Journal of Medical and Biological Research. Associação Brasileira de Divulgação Científica, v. 42, n. 6, p. 476-486, 2009.
ISSN 0100-879X (Sherpa/Romeo, impact factor)
Publisher Associação Brasileira de Divulgação Científica
Extent 476-486
Access rights Open access Open Access
Type Article
Web of Science ID WOS:000266135800017
SciELO ID S0100-879X2009000600002 (statistics in SciELO)

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