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. Author manuscript; available in PMC: 2020 May 29.
Published in final edited form as: Sci Immunol. 2019 Nov 29;4(41):eaax7965. doi: 10.1126/sciimmunol.aax7965

Fig. 6. JNK1-dependent IL-17 and TGF-β signaling.

Fig. 6.

The binding of IL-17A/F to the IL-17RA/IL-17RC receptor facilitates the recruitment of ACT1 to the receptor, which mediates the activation of JNK1, ERK, p38, and NF-κB (p65/p50) signaling, leading to the production of pro-inflammatory cytokines and chemokines (e.g. CXCL1, IL6). Similarly, TGF-β binds to its receptor (TGFBR1/TGFBR2), leading to the activation of JNK1, ERK, p38, and SMAD (SMAD2/3/4) signaling. This pathway ultimately results in the production of extracellular matrix proteins and regulators (e.g. FN1, IL11). The mutation (yellow star) in JNK1 impairs the JNK1-dependent activation of downstream AP-1 (c-Jun/ATF-2), thereby reducing the JNK1-dependent cellular responses to IL-17 and TGF-β.