Activation of STAT6 by STING is critical for antiviral innate immunity.

Abstract:

:STAT6 plays a prominent role in adaptive immunity by transducing signals from extracellular cytokines. We now show that STAT6 is required for innate immune signaling in response to virus infection. Viruses or cytoplasmic nucleic acids trigger STING (also named MITA/ERIS) to recruit STAT6 to the endoplasmic reticulum, leading to STAT6 phosphorylation on Ser(407) by TBK1 and Tyr(641), independent of JAKs. Phosphorylated STAT6 then dimerizes and translocates to the nucleus to induce specific target genes responsible for immune cell homing. Virus-induced STAT6 activation is detected in all cell-types tested, in contrast to the cell-type specific role of STAT6 in cytokine signaling, and Stat6(-/-) mice are susceptible to virus infection. Thus, STAT6 mediates immune signaling in response to both cytokines at the plasma membrane, and virus infection at the endoplasmic reticulum.

journal_name

Cell

journal_title

Cell

authors

Chen H,Sun H,You F,Sun W,Zhou X,Chen L,Yang J,Wang Y,Tang H,Guan Y,Xia W,Gu J,Ishikawa H,Gutman D,Barber G,Qin Z,Jiang Z

doi

10.1016/j.cell.2011.09.022

subject

Has Abstract

pub_date

2011-10-14 00:00:00

pages

436-46

issue

2

eissn

0092-8674

issn

1097-4172

pii

S0092-8674(11)01083-X

journal_volume

147

pub_type

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