Mechanisms of nuclear receptor-mediated control of TH17 differntiation

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We recently demonstrated that activation of the nuclear receptor PPAR! in CD4+ T cells controlled TH17 differentiation in a T cell-intrinsic fashion, hence suppressing CNS autoimmunity. We now plan to assess whether another nuclear receptor, i.e. LXR" also controls TH17 differentiation, and whether endogenous ligands for the nuclear receptors PPAR! and LXR" produced by antigen-presenting cells are operative in controlling TH17 differentiation. In a second part, we will analyze the molecular mechanisms of nuclear receptor-mediated control of TH17 differentiation, such as transrepression and control of T cell metabolism.