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Work model for TIGIT/PVR-mediated suppression of IFN-γ production in NK cells. With TIGIT/PVR engagement, cytoplasmic TIGIT was phosphorylated at Tyr-225 and Tyr-231 residues. Phosphorylated Tyr-225 recruits adaptor protein β-arrestin 2, which further mediates recruitment of SHIP1. Finally, SHIP1 impairs TRAF6 autoubiquitination to inhibit NF-κB activation, leading to suppression of IFN-γ production in NK cells.
