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    Prostaglandin E2 suppresses the differentiation of retinoic acid-producing dendritic cells in mice and humans.

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    Author
    Stock, A; Booth, S; Cerundolo, V
    Date
    2011-04-11
    Source Title
    Journal of Experimental Medicine
    Publisher
    Rockefeller University Press
    University of Melbourne Author/s
    Stock, Angus
    Affiliation
    Medical Biology (W.E.H.I.)
    Metadata
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    Document Type
    Journal Article
    Citations
    Stock, A., Booth, S. & Cerundolo, V. (2011). Prostaglandin E2 suppresses the differentiation of retinoic acid-producing dendritic cells in mice and humans.. J Exp Med, 208 (4), pp.761-773. https://doi.org/10.1084/jem.20101967.
    Access Status
    Open Access
    URI
    http://hdl.handle.net/11343/257147
    DOI
    10.1084/jem.20101967
    Open Access at PMC
    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3135350
    Abstract
    The production of retinoic acid (RA) by dendritic cells (DCs) is critical for the induction of gut-tropic immune responses by driving the expression of intestinal-specific homing receptors, such as α4β7 and CCR9, upon T and B cell activation. However, how RA production is regulated during DC development remains unclear. We describe an unexpected role for prostaglandin E2 (PGE2) as a negative regulator of retinal dehydrogenases (RALDH), the enzymes responsible for RA synthesis. The presence of PGE2 during DC differentiation inhibited RALDH expression in mouse and human DCs, abrogating their ability to induce CCR9 expression upon T cell priming. Furthermore, blocking PGE2 signaling increased the frequency of RALDH(+) DCs in vitro, and reducing PGE2 synthesis in vivo promoted the systemic emergence of RA-producing DCs and the priming of CCR9(+) T cells in nonintestinal sites such as the spleen. Finally, we found that PGE2 stimulated the expression of the inducible cyclic AMP early repressor, which appears to directly inhibit RALDH expression in DCs, thus providing mechanistic insight into how PGE2 signaling down-modulates RALDH. Given the role of PGE2 in regulating the development of RA-producing DCs, modulating this pathway may prove a novel means to control the development of gut-tropic immune responses.

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