| Literature DB >> 31344598 |
Xi-Qiu Xu1, Yu Liu1, Biao Zhang1, Hang Liu1, Dan-Dan Shao1, Jin-Biao Liu1, Xu Wang2, Li-Na Zhou2, Wen-Hui Hu2, Wen-Zhe Ho3.
Abstract
Interleukin (IL)-22, a member of the IL-10 family, plays a role in antiviral immune responses to a number of viral infections. However, it is unclear whether IL-22 is involved in the mucosal immunity against herpes simplex virus 2 (HSV-2) infection in the female reproductive tract (FRT). In this study, we studied whether IL-22 could inhibit HSV-2 infection of human cervical epithelial cells (End1/E6E7 cells). We showed that End1/E6E7 cells express the functional IL-22 receptor complex (IL-22R1 and IL-10R2). When treated with IL-22, End1/E6E7 cells expressed the higher levels of IFN-stimulated genes (ISGs: ISG15, ISG56, OAS-1, OAS-2, and Mx2) than untreated cells. In addition, IL-22-treated cells produced higher levels of the tight junction proteins (ZO-1 and Occludin) than untreated cells. Mechanistically, IL-22 could activate the JAK/STAT signaling pathway by inducing the phosphorylation of STAT1 and STAT3. These observations indicate the potential of IL-22 as an anti-HSV-2 agent in the FRT mucosal innate immunity against HSV-2 infection.Entities:
Keywords: HSV-2; Human cervical epithelial cells; IFN-stimulated gene; IL-22; Signal transducers and activators of transcription; Tight junction proteins
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Year: 2019 PMID： 31344598 PMCID： PMC6739152 DOI： 10.1016/j.cyto.2019.154776
Source DB: PubMed Journal: Cytokine ISSN： 1043-4666 Impact factor: 3.861