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0Recent medical research indicates that HER2+ breast cancer often resists standard treatments due to an immunosuppressive tumor microenvironment driven by the TIGIT signaling pathway. This study identifies that TIGIT, an inhibitory receptor, interacts with ligands like CD112 on cancer cells to disable CD8+ T cells, leading to poor clinical outcomes. By combining anti-HER2 therapy with TIGIT blockade, researchers successfully reinvigorated the immune response and restricted tumor growth in mouse models. The central mechanism for this recovery is the restoration of the costimulatory receptor CD226, which enhances cytotoxicity and IFN-γ production. Consequently, the presence of CD8+CD226+ T cells serves as a vital biomarker for predicting patient survival and monitoring treatment efficacy. These findings offer a promising immunotherapeutic strategy to overcome drug resistance in aggressive breast cancer subtypes.
References:
Zhang L, Li J, Xiu B, et al. Restoring the CD226 in CD8+ T cells overcomes TIGIT-refractory immunity in HER2+ breast cancer[J]. Cell Death & Disease, 2026.
