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. Author manuscript; available in PMC: 2020 Nov 1.
Published in final edited form as: Cytokine. 2019 Jul 22;123:154776. doi: 10.1016/j.cyto.2019.154776

Fig. 8. Schematic diagram of mechanisms for IL-22-mediated HSV-2 inhibition in human cervical epithelial cells.

Fig. 8.

Activated Th cell and NK cell subsets are the primary sources of IL-22 which can bind to the dimeric IL-22R complex (both IL- 22R1 and IL-10R2), resulting in the signal transduction of JAK-STAT pathway in human cervical epithelial cells. Through facilitating the phosphorylation of STAT1, IL-22 induces IFN-stimulated genes (ISG15, ISG56, OAS-1, OAS-2, and Mx2) that have the ability to block HSV-2 DNA transport to cell nuclear and inhibit viral translation, assembly and release. In addition, through the binding to the receptors on human cervical epithelial cells, IL-22 induces the expression of the tight junction proteins (ZO-1 and Occludin), the key cell membrane components for the cell integrity.