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
Celljournal_title
Cellauthors
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 Zdoi
10.1016/j.cell.2011.09.022subject
Has Abstractpub_date
2011-10-14 00:00:00pages
436-46issue
2eissn
0092-8674issn
1097-4172pii
S0092-8674(11)01083-Xjournal_volume
147pub_type
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