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Part of the book series: Progress in Inflammation Research ((PIR))

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Abstract

The vitamin A metabolite, retinoic acid (RA), and transforming growth factor-beta (TGF-β) 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-β mediates the direct inhibition of TH1 and TH2 cytokine polarization concomitant with the generation of regulatory T cells (Tregs), and 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-γ synthesis. Additionally, RA has been shown to efficiently promote gut tropism. We described RA as a key modulator of TGF-β-driven immune deviation capable of suppressing TH17 differentiation while promoting Foxp3+ Treg generation. More recently, RA signaling was also shown to be essential for efficient intestinal immune responses. Here we will discuss how RA can affect mucosal immune regulation.

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Correspondence to Hilde Cheroutre .

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Mucida, D., Cheroutre, H. (2013). Retinoic Acid in Mucosal Immune Regulation. In: Quesniaux, V., Ryffel, B., Padova, F. (eds) IL-17, IL-22 and Their Producing Cells: Role in Inflammation and Autoimmunity. Progress in Inflammation Research. Springer, Basel. https://doi.org/10.1007/978-3-0348-0522-3_8

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  • DOI: https://doi.org/10.1007/978-3-0348-0522-3_8

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