Anti-cancer immunotherapies entirely changed the therapeutic approach to oncological patients. However, despite the undeniable success of anti-PD-1, PD-L1, and CTLA-4 antibody treatments, their effectiveness is limited either by certain types of malignancies or by the arising problem of cancer resistance. B7H4 (aliases B7x, B7H4, B7S1, VTCN1) is a member of a B7 immune checkpoint family with a distinct expression pattern from classical immune checkpoint pathways. The growing amount of research results seem to support the thesis that B7H4 might be a very potent therapeutic target. B7H4 was demonstrated to promote tumour progression in immune “cold” tumours by promoting migration, proliferation of tumour cells, and cancer stem cell persistence. B7H4 suppresses T cell effector functions, including inflammatory cytokine production, cytolytic activity, proliferation of T cells, and promoting the polarisation of naïve CD4 T cells into induced Tregs. This review aimed to summarise the available information about B7H4, focusing in particular on clinical implications, immunological mechanisms, potential strategies for malignancy treatment, and ongoing clinical trials.
抗癌免疫疗法彻底改变了肿瘤患者的治疗策略。然而,尽管抗PD-1、PD-L1和CTLA-4抗体疗法取得了显著成效,但其疗效仍受限于特定肿瘤类型及日益突出的肿瘤耐药性问题。B7H4(亦称B7x、B7H4、B7S1、VTCN1)作为B7免疫检查点家族成员,其表达模式与经典免疫检查点通路存在显著差异。日益增多的研究证据表明,B7H4可能成为极具潜力的治疗靶点。研究证实,在免疫"冷"肿瘤中,B7H4通过促进肿瘤细胞迁移增殖及维持肿瘤干细胞特性来驱动肿瘤进展。该分子能抑制T细胞效应功能,包括炎症因子产生、细胞溶解活性、T细胞增殖,并促进初始CD4 T细胞向诱导性调节性T细胞分化。本文旨在系统综述B7H4的研究进展,重点关注其临床意义、免疫学机制、恶性肿瘤治疗潜在策略及正在进行中的临床试验。