CIAP1/2 antagonization by SMAC mimetic induces non-canonical NF-κB mediated TH 17cell homotypic interactions and increases their resistance to shear stress.

Abstract

SMAC antagonization of cIAP1/2 in TH 17cells upregulates cell adhesion and cytoskeleton genes through the NIK-RelB and p52 axis. SMAC also increases the homotypic interactions of TH 17cells through a non-canonical NF-κB- and integrin-mediated mechanism resulting in increased ability of TH 17cells to withstand shear stress.