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. Author manuscript; available in PMC: 2013 Nov 13.
Published in final edited form as: Immunol Rev. 2009 May;229(1):10.1111/j.1600-065X.2009.00782.x. doi: 10.1111/j.1600-065X.2009.00782.x

Fig. 2. Role of tumor necrosis factor receptor-associated factors (TRAFs) 2 and 3 in the inhibition of non-canonical nuclear factor κB (NFκB) pathway.

Fig. 2

Under non-stimulation, TRAF2 and TRAF3 form a complex with cellular inhibitor of apoptosis 1 and 2 (cIAP1 and cIAP2) and NFκB-inducing kinase (NIK). cIAP1/2 degrades NIK, ablating the non-canonical NFκB pathway (39, 40). After CD40/CD40L engagement, the complex is destabilized, permitting the release of NIK from the complex inducing the non-canonical NFκB signaling. Furthermore, it induced the recruitment of TRAF2 and TRAF3 to CD40 tail and the degradation of TRAF3 by cIAP1/2 proteins.