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Abstract
A lineage of CD4+ T cells known as Th17 cells, which are derived by exposure of naive CD4+ T cells to IL-6 and TGF-β, have been implicated in several autoimmune diseases. In this issue of the JCI, studies by Acharya et al. and Melton et al. show that TGF-β is activated at the DC/CD4+ T cell synapse by αv integrins and that this activation is required for Th17 differentiation and autoimmunity in the central nervous system. Thus, these studies offer a potential therapeutic target in fighting autoimmune diseases.
Authors
Derek A. Pociask, Jay K. Kolls
Figure 1
Schematic representation of Th17 differentiation.
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Two studies in this issue of the JCI (10 , 11 ) demonstrate that TGF-β is activated at the DC/CD4+ T cell synapse by αv integrins and that this activation is required for Th17 differentiation in vitro. Moreover, mice lacking αv integrins on DCs fail to develop EAE, a disease mediated by Th17 cells.
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ISSN: 0021-9738 (print), 1558-8238 (online)