Reciprocal TH17 and regulatory T cell differentiation mediated by retinoic acid
- PMID: 17569825
- DOI: 10.1126/science.1145697
Reciprocal TH17 and regulatory T cell differentiation mediated by retinoic acid
Abstract
The cytokine transforming growth factor-beta (TGF-beta) converts naïve 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 naïve T lymphocytes into proinflammatory IL-17 cytokine-producing T helper 17 (T(H)17) 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 T(H)17 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.
Comment in
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Literature watch: implications for transplantation. AHR and tryptophan catabolism: putting the effector T-cell response to sleep.Am J Transplant. 2012 Apr;12(4):801. doi: 10.1111/j.1600-6143.2012.04058.x. Am J Transplant. 2012. PMID: 22458381 No abstract available.
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