CD276/B7-H3

CD276/B7-H3 is a member of the B7 family of immune checkpoint molecules and plays an important role in regulating immune responses. As a co-stimulatory/co-inhibitory protein, it affects both adaptive and innate immune responses. CD276/B7-H3 was first discovered on dendritic cells and is widely expressed in various tumor tissues, including breast cancer, lung cancer, ovarian cancer, and gastric cancer. Its upregulation is often associated with poor prognosis, increased tumor invasiveness, and metastasis.
CD276/B7-H3 has a dual role in the immune system. It can act as a co-stimulatory molecule, enhancing T cell proliferation and cytotoxicity in certain cases, but it can also function as a co-inhibitory molecule by suppressing T cell activity and promoting immune evasion by tumors, thus contributing to tumor progression and metastasis. This dual function makes CD276/B7-H3 a promising target in cancer immunotherapy research. In the tumor microenvironment, its expression is linked to immune suppression, further promoting tumor growth and metastasis.
Research strategies targeting B7-H3 include monoclonal antibodies, antibody-drug conjugates (ADC), bispecific antibodies, and chimeric antigen receptor (CAR) T cell therapies. These strategies have demonstrated promising results in preclinical studies, enhancing immune responses and inhibiting tumor growth in various tumor models^[1].