Immunotherapy has emerged as a major therapeutic modality in oncology. Currently, however, the majority of patients with cancer do not derive benefit from these treatments. Vascular abnormalities are a hallmark of most solid tumours and facilitate immune evasion. These abnormalities stem from elevated levels of proangiogenic factors, such as VEGF and angiopoietin 2 (ANG2); judicious use of drugs targeting these molecules can improve therapeutic responsiveness, partially owing to normalization of the abnormal tumour vasculature that can, in turn, increase the infiltration of immune effector cells into tumours and convert the intrinsically immunosuppressive tumour microenvironment (TME) to an immunosupportive one. Immunotherapy relies on the accumulation and activity of immune effector cells within the TME, and immune responses and vascular normalization seem to be reciprocally regulated. Thus, combining antiangiogenic therapies and immunotherapies might increase the effectiveness of immunotherapy and diminish the risk of immune-related adverse effects. In this Perspective, we outline the roles of VEGF and ANG2 in tumour immune evasion and progression, and discuss the evidence indicating that antiangiogenic agents can normalize the TME. We also suggest ways that antiangiogenic agents can be combined with immune-checkpoint inhibitors to potentially improve patient outcomes, and highlight avenues of future research.

免疫疗法已成为肿瘤学中的一种主要治疗方式。但是，目前，大多数癌症患者并未从这些治疗中受益。血管异常是大多数实体瘤的标志，可促进免疫逃逸。这些异常源于血管生成因子，例如VEGF和血管生成素2（ANG2）的升高。明智地使用靶向这些分子的药物可以改善治疗反应性，部分原因是异常肿瘤脉管系统的正常化，进而可以增加免疫效应细胞向肿瘤的浸润并将固有免疫抑制性肿瘤微环境（TME）转化为免疫支持性。免疫疗法依赖于TME内免疫效应细胞的积累和活性，免疫反应和血管正常化似乎相互调节。因此，将抗血管生成疗法与免疫疗法相结合可提高免疫疗法的有效性，并降低免疫相关不良反应的风险。在此观点中，我们概述了VEGF和ANG2在肿瘤免疫逃逸和进展中的作用，并讨论了表明抗血管生成剂可以使TME正常化的证据。我们还提出了将抗血管生成剂与免疫检查点抑制剂联合使用以潜在改善患者预后的方法，并着重指出了未来研究的途径。我们概述了VEGF和ANG2在肿瘤免疫逃逸和进展中的作用，并讨论了表明抗血管生成剂可以使TME正常化的证据。我们还提出了将抗血管生成剂与免疫检查点抑制剂联合使用以潜在改善患者预后的方法，并着重指出了未来研究的途径。我们概述了VEGF和ANG2在肿瘤免疫逃逸和进展中的作用，并讨论了表明抗血管生成剂可以使TME正常化的证据。我们还提出了将抗血管生成剂与免疫检查点抑制剂联合使用以潜在改善患者预后的方法，并着重指出了未来研究的途径。