Integral role of integrins in Th17 development

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.

Figure 1. Schematic representation of Th17 differentiation.

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.