Tumor Necrosis Factor (TNF) Receptor Expression Determines Keratinocyte Fate upon Stimulation with TNF-Like Weak Inducer of Apoptosis

Figure 7

Diagram of the function of the Fn14-TRAF2-TNFR signaling axis. TWEAK/Fn14 interaction acts independently or cooperates with TNF-α in triggering TNFR-mediated signals. In the TNFR1-predominant cells (such as normal keratinocytes), TWEAK induces cell death through activation of the TRADD and caspase-8 pathways. Conversely, TWEAK induces proliferation of cells that overexpress TNFR2 (such as HPV-infected keratinocytes). The Fn14-TRAF2-TNFR axis is central to TWEAK’s regulation of cell fate.