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On taking the STING out of immune activation
Author(s) -
Banete Andra,
Seaver Kyle,
Bakshi Devyani,
Gee Katrina,
Basta Sameh
Publication year - 2018
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1002/jlb.2mir0917-383r
Subject(s) - sting , stimulator of interferon genes , biology , interferon , immune system , irf3 , innate immune system , immunology , signal transduction , immunity , interferon regulatory factors , interferon type i , transcription factor , signal transducing adaptor protein , cytotoxic t cell , irf7 , microbiology and biotechnology , cancer research , gene , genetics , engineering , in vitro , aerospace engineering
Nearly a decade ago, an endoplasmic reticulum (ER) adaptor protein called stimulator of interferon genes (STING) was found to be critical in the induction of type I IFN production in response to DNA virus infection. STING functions by sensing cytoplasmic DNA and activates key transcription factors, including IFN regulatory factor (IRF)‐3 and IRF7, to initiate type I IFN expression. Type I IFNs are vital in immunity against viral infections and can influence cancer cell proliferation, migration, and apoptosis. Several studies have shown that STING activation results in potent antitumor activity by generating strong tumor‐specific cytotoxic T‐cell responses. Moreover, compared with wild‐type, STING‐knockout mice show greater susceptibility to viral infections. In this review, we discuss the importance of STING signaling during the induction of immune responses, especially those associated with type I IFN in viral infections and tumor immunity. Furthermore, we highlight recent data that unravel how the STING signaling pathway can be negatively regulated.