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IL-22 Suppresses HSV-2 Replication in Human Cervical Epithelial Cells

Xi-Qiu Xu, Yu Liu, Biao Zhang, Hang Liu, Dan-Dan Shao, Jin-Biao Liu, Xu Wang, Li-Na Zhou, Wen-Hui Hu, Wen-Zhe Ho

Cytokine. 2019 Nov;123:154776.

PMID: 31344598

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.

Chemicals Related in the Paper:

Catalog Number Product Name Structure CAS Number Price
IAR42413388 IL-22 human IL-22 human Price
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