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BATF2 inhibits immunopathological Th17 responses by suppressing Il23a expression during Trypanosoma cruzi infection.

Authors: Kitada, Shoko  Kayama, Hisako  Okuzaki, Daisuke  Koga, Ritsuko  Kobayashi, Masao  Arima, Yasunobu  Kumanogoh, Atsushi  Murakami, Masaaki  Ikawa, Masahito  Takeda, Kiyoshi 
Citation: Kitada S, etal., J Exp Med. 2017 May 1;214(5):1313-1331. doi: 10.1084/jem.20161076. Epub 2017 Mar 29.
Pubmed: (View Article at PubMed) PMID:28356392
DOI: Full-text: DOI:10.1084/jem.20161076

Inappropriate IL-17 responses are implicated in chronic tissue inflammation. IL-23 contributes to Trypanosoma cruzi-specific IL-17 production, but the molecular mechanisms underlying regulation of the IL-23-IL-17 axis during T. cruzi infection are poorly understood. Here, we demonstrate a novel function of BATF2 as a negative regulator of Il23a in innate immune cells. IL-17, but not IFN-γ, was more highly produced by CD4+ T cells from spleens and livers of T. cruzi-infected Batf2-/- mice than by those of wild-type mice. In this context, Batf2-/- mice showed severe multiorgan pathology despite reduced parasite burden. T. cruzi-induced IL-23 production was increased in Batf2-/- innate immune cells. The T. cruzi-induced enhanced Th17 response was abrogated in Batf2-/-Il23a-/- mice. The interaction of BATF2 with c-JUN prevented c-JUN-ATF-2 complex formation, inhibiting Il23a expression. These results demonstrate that IFN-γ-inducible BATF2 in innate immune cells controls Th17-mediated immunopathology by suppressing IL-23 production during T. cruzi infection.


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RGD Object Information
RGD ID: 39457935
Created: 2020-10-08
Species: All species
Last Modified: 2020-10-08
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.