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
Language English
Sponsor Crohn's and Colitis Foundation of America
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
Access rights Open access Open Access
Type Review
Web of Science ID WOS:000265700100003

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