Tumor Immunotherapy Targeting B7-H3: From Mechanisms to Clinical Applications.

Abstract

B7-H3 (CD276) is an immune checkpoint from the B7 family of molecules and is abnormally expressed in tumor cells as a co-inhibitory molecule to promote tumor progression. Within the tumor microenvironment (TME), B7-H3 promotes tumor progression by impairing the T cell response, driving the polarization of tumor-associated macrophages (TAMs) to M2 phenotype, and inhibiting the function of other immune cells. In addition, B7-H3 promotes tumor cell proliferation, migration, invasion, metabolism disorder, angiogenesis, and resistance to treatment to promote tumor progression through its non-immunological functions. Immunotherapy targeting B7-H3, as well as combinations with other immune checkpoint therapies, have shown certain efficacy. In this review, we synthesizes the expression of B7-H3 and its mechanism to promote tumor progression through inducing immunomodulation and non-immunological functions, as well as its role of B7-H3 in tumor therapy, aiming to provide a reference for the clinical treatment of tumors.