Journal
SCIENCE
Volume 317, Issue 5835, Pages 256-260Publisher
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.1145697
Keywords
-
Categories
Funding
- NIAID NIH HHS [R01 AI050265-06] Funding Source: Medline
Ask authors/readers for more resources
The cytokine transforming growth factor-beta (TGF-beta) converts naive T cells into regulatory T (Treg) cells that prevent autoimmunity. However, in the presence of interleukin-6 (IL-6), TGF-beta has also been found to promote the differentiation of naive T lymphocytes into proinflammatory IL-17 cytokine-producing T helper 17 (TH17) cells, which promote autoimmunity and inflammation. This raises the question of how TGF-beta can generate such distinct outcomes. We identified the vitamin A metabolite retinoic acid as a key regulator of TGF-beta-dependent immune responses, capable of inhibiting the IL-6-driven induction of proinflammatory TH17 cells and promoting anti-inflammatory Treg cell differentiation. These findings indicate that a common metabolite can regulate the balance between pro- and anti-inflammatory immunity.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available