cIAP1/2 antagonization by SMAC mimetic induces non-canonical NF-κB mediated T 17 cell homotypic interactions and increases their resistance to shear stress.

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