Journal
JOURNAL OF IMMUNOLOGY
Volume 196, Issue 12, Pages 5101-5111Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.1600212
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Funding
- Ministry of Science and Technology of China [2012CB910201, 2014CB542600]
- National Natural Science Foundation of China [31521091, 91429304, 31400743]
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Viral infection triggers induction of antiviral cytokines and effectors, which are critical mediators of innate antiviral immune response. It has been shown that the processing body-associated protein LSm14A is involved in the induction of antiviral cytokines in cell lines but in vivo evidence is lacking. By generating LSm14A-deficient mice, in this study, we show that LSm14A plays a critical and specific role in the induction of antiviral cytokines in dendritic cells (DCs) but not in macrophages and fibroblasts. Induction of antiviral cytokines triggered by the DNAviruses HSV-1 and murid herpesvirus 68 and the RNAvirus vesicular stomatitis virus but not Sendai virus was impaired in Lsm14a 2/2 DCs, which is correlated to the functions of the adaptor protein MITA/STING in the antiviral signaling pathways. LSm14A deficiency specifically downregulated MITA/STING level in DCs by impairing its nuclear mRNA precursor processing and subsequently impaired antiviral innate and adaptive immune responses. Our findings reveal a nuclear mRNA precursor processing and cell-specific regulatory mechanism of antiviral immune responses.
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