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Prostaglandin E2 suppresses antifungal immunity by inhibiting interferon regulatory factor 4 function and interleukin-17 expression in T cells.

Abstract：

:T helper 17 (Th17) cells play an important role in mucosal host defense through production of the signature cytokines IL-17 and IL-22. Prostaglandin E2 (PGE2) has been shown to enhance IL-17 production by mature Th17 cells. However, when present during Th17 cell differentiation, we found that PGE2 inhibited the transcription factor IRF4 and suppressed production of IL-17 but not IL-22. We show that IRF4 was required for IL-17 expression but inhibited IL-22 expression, highlighting the potential for discordant regulation of these two cytokines in Th17 cells. The pathogenic fungus Cryptococcus neoformans produces PGE2, and we found that it uses PGE2- and IRF4-dependent mechanisms to specifically inhibit induction of IL-17 during Th17 cell differentiation. Blockade of host PGE2 during infection led to increased IL-17 production from CD4(+) T cells and increased survival of mice. These findings suggest that host- or pathogen-derived PGE2 can act directly on Th17 cells during differentiation to inhibit IL-17-dependent antimicrobial responses.

journal_name

Immunity

journal_title

Immunity

authors

Valdez PA,Vithayathil PJ,Janelsins BM,Shaffer AL,Williamson PR,Datta SK

doi

10.1016/j.immuni.2012.02.013

subject

Has Abstract

pub_date

2012-04-20 00:00:00

pages

668-79

issue

4

eissn

1074-7613

issn

1097-4180

pii

S1074-7613(12)00122-7

journal_volume

36

pub_type

杂志文章

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