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For many years, CD4+ effector T cells were categorized into two subsets: T helper type 1 (Th1) and type 2 (Th2) cells. More recent research has refined this model, delineating further subsets; in particular, Th17 cells, activated CD4+ T cells characterised by the production of the cytokine IL-17. Autoantigen-specific Th17 cells are associated with pathology in a number of animal models of organ-specific autoimmune disease and evidence is mounting that Th17 cells are also critical in human autoimmunity. Retinoids, a family of compounds that bind to and activate retinoic acid receptors (RARs and RXRs), are able to alter CD4+ T cell differentiation in vitro though agonism and antagonism of a range of retinoid receptors. For example, all-trans retinoic acid (ATRA) inhibits Th17 differentiation and instead promotes the upregulation of Foxp3, a key transcription factor in regulatory T cells. Importantly, treatment with retinoids can modulate Th17-mediated autoimmunity: experimental autoimmune encephalomyelitis (EAE), the murine model of multiple sclerosis (MS), is ameliorated by ATRA administration due to suppression of both the differentiation and the function of Th17 cells. In this review, we discuss the unveiled molecular mechanism and the possible clinical application of retinoids for the treatment of human Th17-mediated autoimmune diseases.

Retinoid signals and Th17-mediated pathology