Abstract
TIGIT (T-cell immunoglobulin and ITIM domain), which is expressed on T and NK cells, can interact with its ligands (i.e., CD155 and CD122), leading to inhibitory signaling in T cells and promoting exhaustion of lymphocytes. Although TIGIT is considered as a promising immune checkpoint molecule, the single-agent efficacy of anti-TIGIT therapy is limited. TGF-β (Transforming growth factor-beta), serves as an immune regulator in the tumor microenvironment (TME), is elevated in various tumor types and contributes to the resistance to checkpoint inhibitors.
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