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. 2022 Mar 30;12:844260. doi: 10.3389/fonc.2022.844260

Figure 2.

Figure 2

The comprehensive mechanisms of TIGIT/CD155 axis mediated in the immune system in various models and biological contexts. (A) After TIGIT expressed on NK cells binds to CD155, the intracellular immunoreceptor (ITT)-like motif of TIGIT is phosphorylated at Tyr255 and interacts with Grb2, which terminates MAPK and PI3K signaling via recruiting SHIIP1, leading to the inhibition of NK cell function. (B) TIGIT/CD155 axis directly induces CD8+T cell exhaustion by recruiting SHIP1 and SHP2 phosphatase. (C) Tumor cells restrict NK and CD8+T cell activity using the Fap2 protein of F.nucleatum bacteria to interact with TIGIT. (D) The deletion of CD226 enhances TIGIT/CD155 signaling, thereby maintaining the immunosuppressive function of Tregs with the inhibition of the AKT-mTORC1 pathway. (E) After TIGIT/CD155 ligation, the transcription factor CEBPα promotes the transcription of the soluble effector molecule fibrinogen-like protein 2 (Fgl2), thereby the hypersecretion of Fgl2 in Tregs facilitates the suppression of pro-inflammatory Th1 and Th17 cells. (F) The binding of CD155 to TIGIT on dendritic cells (DC) induces the production of IL-10 and inhibits the production of IL-12, which directly leads to the DC maturation and indirectly reduces the proliferation and function of T cells. (G) TIGIT expressed on specific B cell subsets binds to CD155 expressed on DC, leading to the decreased expression of IL-12, IL-16 and CCR7, thereby inhibiting the maturation and pro-inflammatory response of DC.