Retinoic acid in mucosal immune-regulation
The vitamin A metabolite, retinoic acid (RA), and transforming growth factor-ß (TGF-ß) are both abundantly produced in the gut and are known to play significant roles in a variety of developmental processes, including the differentiation of lymphocyte lineages. TGF-ß mediates the direct inhibition of Th1 and Th2 cytokine polarization concomitant with the generation of regulatory T cells (Tregs). Paradoxically, along with inflammatory cytokines such as IL-6, it also induces the differentiation of pro-inflammatory IL-17-producing CD4 helper T cells (Th17). RA, in contrast, is able under certain conditions to stimulate Th2 differentiation and it is a profound inhibitor of IFN-g synthesis. Additionally, RA has been shown to efficiently promote gut tropism. We recently described RA as a key modulator of TGF-ß-driven immune deviation capable of suppressing Th17 differentiation while promoting Foxp3+Treg generation. Here we discuss how RA can affect mucosal immune regulation.
KeywordsRetinoic Acid Treg Cell Oral Tolerance Retinoic Acid Signaling Oral Tolerance Induction
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