Abstract：
:Viral infection triggers host innate immune responses that result in the production of various cytokines including type I interferons (IFN), activation of inflammasomes, and programmed cell death of the infected cells. Tight control of inflammatory cytokine production is crucial for the triggering of an effective immune response that can resolve the infection without causing host pathology. In examining the inflammatory response of Asc-/- and Casp1-/- macrophages, we found that deficiency in these molecules resulted in increased IFN production upon DNA virus infection, but not RNA virus challenge. Investigation of the underlying mechanism revealed that upon canonical and non-canonical inflammasome activation, caspase-1 interacted with cyclic GMP-AMP (cGAMP) synthase (cGAS), cleaving it and dampening cGAS-STING-mediated IFN production. Deficiency in inflammasome signaling enhanced host resistance to DNA virus in vitro and in vivo, and this regulatory role extended to other inflammatory caspases. Thus, inflammasome activation dampens cGAS-dependent signaling, suggesting cross-regulation between intracellular DNA-sensing pathways.
journal_name
Immunityjournal_title
Immunityauthors
Wang Y,Ning X,Gao P,Wu S,Sha M,Lv M,Zhou X,Gao J,Fang R,Meng G,Su X,Jiang Zdoi
10.1016/j.immuni.2017.02.011subject
Has Abstractpub_date
2017-03-21 00:00:00pages
393-404issue
3eissn
1074-7613issn
1097-4180pii
S1074-7613(17)30073-0journal_volume
46pub_type
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