1404-Restoring CD226 to Overcome Refractory Breast Cancer
Recent 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…
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