TWEAK/Fn14 Activation Participates in Skin Inflammation

Figure 2

The diagram for the Fn14-TRAF-TNFR axis. sTWEAK binding to Fn14 recruits TRAF2 and cIAP1/2 to form cIAP-TRAF2 complex. The recruitment of TNFR1, TRADD, and FADD initiates apoptotic signaling by the recruitment and activation of caspase-8, while TNFR2 induces cell survival/antiapoptotic signals through NF-κB activation. NF-κB activation upregulates expression of multiple cellular genes that encode proinflammatory cytokines such as TNF-α. TWEAK may independently act or cooperate with TNF-α in regulating the TNFR-mediated cell fate.