Yeo, Jinah Ko, Minkyung Lee, Dong-Hee Park, Yoon Jin, Hyung-seung 2024-01-19T15:04:59Z 2024-01-19T15:04:59Z 2022-01-10 2021-03 1424-8247 https://pubs.kist.re.kr/handle/201004/117303 Tumors escape immune surveillance by inducing various immunosuppressive pathways, including the activation of inhibitory receptors on tumor-infiltrating T cells. While monoclonal antibodies (mAbs) blocking programmed cell death 1 (PD-1), programmed death-ligand 1 (PD-L1), and cytotoxic T lymphocyte-associated antigen 4 (CTLA-4) have been approved for multiple cancer indications, only a subset of patients benefit from immune checkpoint blockade therapies, highlighting the need for additional approaches. Therefore, the identification of new target molecules acting in distinct or complementary pathways in monotherapy or combination therapy with PD-1/PD-L1 blockade is gaining immense interest. T cell immunoreceptor with Ig and immunoreceptor tyrosine-based inhibitory motif (ITIM) domains (TIGIT) has received considerable attention in cancer immunotherapy. Recently, anti-TIGIT mAb (tiragolumab) has demonstrated promising clinical efficacy in non-small cell lung cancer treatment when combined with an anti-PD-L1 drug (Tecentriq), leading to phase III trial initiation. TIGIT is expressed mainly on T and natural killer cells; it functions as an inhibitory checkpoint receptor, thereby limiting adaptive and innate immunity. CD226 competes for binding with the same ligands with TIGIT but delivers a positive stimulatory signal to the immune cells. This review discusses the recent discoveries regarding the roles of TIGIT and CD226 in immune cell function and their potential application in cancer immunotherapy. English MDPI TIGIT/CD226 Axis Regulates Anti-Tumor Immunity Article 10.3390/ph14030200 1 PHARMACEUTICALS, v.14, no.3 PHARMACEUTICALS 14 3 scie scopus 000634097200001 2-s2.0-85102263342 Chemistry, Medicinal Pharmacology & Pharmacy Pharmacology & Pharmacy Review cancer immunotherapy immune checkpoint blockade CD226 TIGIT PVR