期刊
IMMUNITY
卷 34, 期 3, 页码 396-408出版社
CELL PRESS
DOI: 10.1016/j.immuni.2011.03.005
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资金
- Rita Allen Foundation
- National Institute of Arthritis, Musculoskeletal, and Skin Diseases [KO1 AR053595, RO1 AR060723]
- Arthritis Foundation
- National Research Fund, Luxembourg
- European Commission
TGF-beta 1 is a regulatory cytokine that has an important role in controlling T cell differentiation. T cell-produced TGF-beta 1 acts on T cells to promote Th17 cell differentiation and the development of experimental autoimmune encephalomyelitis (EAE). However, the exact TGF-beta 1-producing T cell subset required for Th17 cell generation and its cellular mechanism of action remain unknown. Here we showed that deletion of the Tgfb1 gene from activated T cells and Treg cells, but not Treg cells alone, abrogated Th17 cell differentiation, resulting in almost complete protection from EAE. Furthermore, differentiation of T cells both in vitro and in vivo demonstrated that TGF-beta 1 was highly expressed by Th17 cells and acted in a predominantly autocrine manner to maintain Th17 cells in vivo. These findings reveal an essential role for activated T cell-produced TGF-beta 1 in promoting the differentiation of Th17 cells and controlling inflammatory diseases.
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