More stories on Th17 cells

Author Basso, Alexandre Salgado Autor UNIFESP Google Scholar
Cheroutre, Hilde Google Scholar
Mucida, Daniel Google Scholar
Institution La Jolla Inst Allergy & Immunol
Universidade Federal de São Paulo (UNIFESP)
Abstract For more than two decades, immunologists have been using the so-called Th1/Th2 paradigm to explain most of the phenomena related to adaptive immunity. the Th1/Th2 paradigm implied the existence of two different, mutually regulated, CD4(+) T helper subsets: Th1 cells, driving cell-mediated immune responses involved in tissue damage and fighting infection against intracellular parasites; and Th2 cells that mediate IgE production and are particularly involved in eosinophilic inflammation, allergy and clearance of helminthic infections. A third member of the T helper set, IL-17-producing CD4(+) T cells, now called Th17 cells, was recently described as a distinct lineage that does not share developmental pathways with either Th1 or Th2 cells. the Th17 subset has been linked to autoimmune disorders, being able to produce IL-17, IL-17F and IL-21 among other inflammatory cytokines. Interestingly, it has been reported that there is not only a cross-regulation among Th1, Th2 and Th17 effector cells but there is also a dichotomy in the generation of Th17 and T regulatory cells. Therefore, Treg and Th17 effector cells arise in a mutually exclusive fashion, depending on whether they are activated in the presence of TGF-beta or TGF-beta plus inflammatory cytokines such as IL-6. This review will address the discovery of the Th17 cells, and recent progress on their development and regulation.
Keywords adaptive immunity
tolerance
IFN-gamma
IL-4
IL-23
TGF-beta
Language English
Sponsor Crohn's and Colitis Foundation of America
NIH
Grant number NIH: RO1 AI050265-06
Date 2009-04-01
Published in Cell Research. New York: Nature Publishing Group, v. 19, n. 4, p. 399-411, 2009.
ISSN 1001-0602 (Sherpa/Romeo, impact factor)
Publisher Nature Publishing Group
Extent 399-411
Origin http://dx.doi.org/10.1038/cr.2009.26
Access rights Open access Open Access
Type Review
Web of Science ID WOS:000265700100003
URI http://repositorio.unifesp.br/handle/11600/31393

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