Fig. 6: MDA5-mediated IFN-β is central to the secretion of CXCL10 while CXCL16 is directly regulated by IRF3. | Cell Death & Disease

Fig. 6: MDA5-mediated IFN-β is central to the secretion of CXCL10 while CXCL16 is directly regulated by IRF3.

From: Intracellular virus sensor MDA5 exacerbates vitiligo by inducing the secretion of chemokines in keratinocytes under virus invasion

Fig. 6: MDA5-mediated IFN-β is central to the secretion of CXCL10 while CXCL16 is directly regulated by IRF3.The alternative text for this image may have been generated using AI.

a The mRNA and secretion levels of IFN-β in HaCaT cells in response to Poly(I:C). b The secretion levels of IFN-β when interfering any of MDA5, MAVS, NF-kB, IRF3 prior to 24 h treatment of Poly(I:C) in HaCaT cells. c The secretion levels of CXCL10 and CXCL16 when treated with Poly(I:C)-pretreated supernatant (Sup) with or without neutralizing the IFN-β by using the IFN-β neutralizing antibody (Neu), detected by ELISA assay. d, e The expression of total JAK, phosphor-JAK, total STAT1, phosphor-STAT1 and MDA5 in HaCaT cells exposed to the Poly(I:C)-pretreated supernatant (Sup), and simultaneously with or without neutralizing IFN-β (Neu) (d) or blocking JAK1-STAT1 pathway with the pretreatment of Tofacitinib (Tofa) (e). f The mRNA and secretion levels of CXCL10 and CXCL16 in HaCaT cells stimulated by recombined human IFN-β (rh IFN-β) or pretreated with Tofacitinib (Tofa), detected by ELISA. g Chromatin immunoprecipitation assay (ChIP) of IRF3 to CXCL16 promoter after the HaCaT cells were treated by Poly(I:C) for 18 h. h The diagram of the pathophysiological process in keratinocytes under the virus invasion. Data are presented as the mean ± SD across three independently performed experiments. **P < 0.01, ***P < 0.001, #P < 0.05, ##P < 0.01. ns, not significant.

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