In:
The Journal of Immunology, The American Association of Immunologists, Vol. 198, No. 1_Supplement ( 2017-05-01), p. 129.20-129.20
Abstract:
RIG-I-like receptors (RLRs) sense non-self RNA, inducing type I IFNs. Type I IFN promotes the expression of IFN-stimulated genes (ISGs), which requires the activation of STAT1. We previously reported that dsRNA induced STAT1 phosphorylation via a type I IFN-independent pathway in addition to the well-known type I IFN-dependent pathway. IKKα is involved in antiviral signaling induced by dsRNA in the RLR-mediated antiviral signaling; however, its role remains uncertain. In this study, we investigated the role of IKKα in RLR signaling, which is essential for antiviral innate immune responses in non-professional antigen-presenting cells, such as epithelial cells. Silencing of IKKα markedly decreased the level of IFN-β and STAT1 phosphorylation in response to dsRNA. However, the inhibition of IKKα did not alter the RLR signaling-mediated dimerization of IRF3 or activation of NFκB. These results suggest a non-canonical role of IKKα in RLR signaling. In addition, STAT1 phosphorylation was inhibited by IKKα knockdown in IFNAR-deficient cells. These results suggest that the dual regulation of STAT1 by IKKα in the RLR-mediated antiviral signaling.
Type of Medium:
Online Resource
ISSN:
0022-1767
,
1550-6606
DOI:
10.4049/jimmunol.198.Supp.129.20
Language:
English
Publisher:
The American Association of Immunologists
Publication Date:
2017
detail.hit.zdb_id:
1475085-5
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