Fig. (3).
The TRL2 pathway is activated by Tollip and results in IRAK suppression. Upon stimulation with IL-1, the Tollip-IRAK-1 complex is recruited to the IL-1 receptor complex causing IRAK-1 phosphorylation, dissociation from Tollip and TRAF6 activation. Tollip overexpression leads to the suppression of NF-kβ inhibition. Negative regulation of TLR signaling by Tollip may therefore serve to limit the production of pro-inflammatory mediators during the inflammation process following an infection.
