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CUTTING EDGE |
* Department of Host Defense and
Exploratory Research for Advanced Technology, Japan Science and Technology Agency, Research Institute for Microbial Diseases, Osaka University, Osaka, Japan; and
Department of Gastroenterology and Hepatology, Graduate School of Medicine and
Graduate School of Biostudies, Kyoto University, Kyoto, Japan
Upon viral infection, host cells trigger antiviral immune responses by inducing type I IFN and inflammatory cytokines. dsRNA generated during viral replication is recognized by the cytoplasmic RNA helicases retinoic acid-inducible gene I and melanoma differentiation-associated gene 5, which interact with an adaptor, IFN-
promoter stimulator-1, to activate the transcription factors NF-
B and IFN regulatory factor 3. In this article we demonstrate that caspase-8 and caspase-10 are involved in these pathways. Both caspases were cleaved during dsRNA stimulation, and overexpression of a cleaved form of these caspases activated NF-B. Knockdown of caspase-10 or caspase-8 in a human cell line resulted in the reduction of inflammatory cytokine production. Cells derived from caspase-8-deficient mice also showed reduced expression of inflammatory cytokines as well as NF-B activation. Furthermore, the Fas-associated death domain protein interacted with these two caspases and IFN- promoter stimulator 1. These results indicate that caspase-8 and caspase-10 are essential components that mediate NF-B-dependent inflammatory responses in antiviral signaling.
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