Abstract
Despite intrinsic resistance to immunotherapy, some NSCLC tumors are susceptible to T-cell-mediated antitumor effects. Targeting multiple cancer immunity processes may enhance response in relapsed or refractory NSCLC. The CD226 Axis includes the T- and NK-cell inhibitory receptors TIGIT, CD96, and PVRIG (CD112R); the T-/NK-cell activating receptor CD226 (DNAM-1); and cognate ligands CD155 (PVR) and CD112. These immune receptors play a critical role regulating antitumor responses. The immune checkpoints TIGIT, CD96, and PVRIG may prevent CD226’s interactions with CD155 and CD112, directly impairing NK- and T-cell function; this impairment reduces antitumor response.
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