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.
Department of Pathology, Feinberg School of Medicine, Northwestern University, Chicago, Illinois, USA.
Jennifer J
JJ
Heller
Ju
J
Qiu
Liang
L
Zhou
D000818:Animals; D015551:Autoimmunity / Q000276:immunology*; D002454:Cell Differentiation / Q000276:immunology; D006801:Humans; D020381:Interleukin-17 / Q000235:genetics / Q000276:immunology; D000071518:Liver X Receptors; D051379:Mice; D057093:Orphan Nuclear Receptors / Q000276:immunology*; D018336:Receptors, Aryl Hydrocarbon / Q000276:immunology; D058504:Th17 Cells / Q000276:immunology* / Q000502:physiology
D020381:Interleukin-17; D000071518:Liver X Receptors; D057093:Orphan Nuclear Receptors; D018336:Receptors, Aryl Hydrocarbon
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