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. Author manuscript; available in PMC: 2017 Jul 19.
Published in final edited form as: Immunity. 2016 Jul 19;45(1):119–130. doi: 10.1016/j.immuni.2016.06.021

Fig. 3. IFNβ production from epidermal keratinocyte in response to LL37 and dsRNA is mediated by MAVS.

Fig. 3

(A–B). RTqPCR of mRNA expression of MAVS, various TLRs and IFNAR1 in KC (NHEK), pDC analyses or cDC (A) (n=3; ratio to GAPDH mRNA is shown), or separated epidermis and dermis from normal human skin (B) (fold changes are shown relative to TLR3) (n=3). (C). RTqPCR analysis of IFNB1 mRNA expression in NHEKs transfected with control siRNA, TLR3 siRNA or MAVS siRNA then stimulated with polyIC with or without LL37 pretreatment. (n=3). (D). RTqPCR analysis of Ifnb1 mRNA expression in LL37/polyIC stimulated mouse KCs isolated from Mavs−/+ HET or Mavs−/− KO littermate mice (n=3). (E). RTqPCR analysis of IFNB1 mRNA expression in NHEKs transfected with control siRNA, TLR3 siRNA or MAVS siRNA then stimulated with LL37 and U1-RNA as indicated (n=3). (F). NHEKs treated with various combination of polyIC and LL37 were co-immunostained with anti-MAVS antibody and mitochondrial tracker (MitoV) or phosphor-tyrosine (pTyr) as indicated. (G). Time course analyses of ISG15 mRNA expression in NHEKs treated with LL37 and polyIC as indicated (n=3). (H–I). ISG15 expression in siRNA mediated silencing of TLR3 or MAVS (H) or IFNB1 or IFNAR1. (I) NHEKs treated with LL37 and polyIC (n=3). (J) Proposed scheme for induction of proinflammatory cytokines and type-1 IFN responsive genes mediated by LL37 and dsRNA mediated through MAVS or TLR3. All error bars indicate mean ± s.e.m. * P<0.05, ** P<0.01, *** P<0.001 (one way Anova). L/P, LL37 and polyIC.