Nuclear receptors take center stage in Th17 cell-mediated autoimmunity.

Liver X receptors (LXRs) are nuclear receptors involved in cholesterol homeostasis. Notably, they are also expressed by T cells and are involved in regulating T cell proliferation and differentiation. In this issue of the JCI, Cui et al. have elucidated the molecular mechanism underlying the effects of LXR activation on a subset of T cells known as Th17 cells in mice and humans. Specifically, they showed that LXR-induced Srebp-1 inhibits Il17 transcription by binding to the Il17 promoter through interaction with the aryl hydrocarbon receptor (Ahr), a transcription factor known to enhance Th17 cell responses.