Poly (ADP-ribose) polymerase (PARP) inhibitors have demonstrated great promise for treating cancers with homologous recombination (HR) defects, such as germline BRCA1/2 mutation. Further studies suggest that PARP inhibitors (PARPi) can also exhibit efficacy in HR-competent cancers, by amplifying the DNA damage and inducing immunogenic cell death, and PARPi lead to increasing tumor neoantigen, upregulation of interferons and PD-L1, and modulation of the tumor microenvironment, which may facilitate a more profound antitumor immune response. Immune checkpoint inhibitors (ICIs) targeting PD-1/PD-L1 or CTLA-4 have achieved impressive success in the treatment of different malignancies. However, only a subset of populations derive clinical benefit, and the biomarkers and resistance mechanisms are not fully understood. Therefore, given that PARPi could potentiate the therapeutic effect of ICIs, PARPi combined with ICIs are becoming an alternative for patients who cannot benefit from ICI monotherapy. In this review, we focus on the mechanisms and immune role of PARPi and discuss the rationale and clinical studies of this combined regimen.

聚（ADP-核糖）聚合酶（PARP）抑制剂已显示出治疗具有同源重组（HR）缺陷（例如种系BRCA1 / 2突变）的癌症的巨大希望。进一步的研究表明，PARP抑制剂（PARPi）还可通过放大DNA损伤并诱导免疫原性细胞死亡而在具有HR活性的癌症中显示功效，并且PARPi会导致肿瘤新抗原增加，干扰素和PD-L1上调以及对肿瘤的调节肿瘤微环境，可能促进更深刻的抗肿瘤免疫反应。靶向PD-1 / PD-L1或CTLA-4的免疫检查点抑制剂（ICI）在治疗各种恶性肿瘤方面取得了令人瞩目的成功。然而，只有一小部分人群获得临床益处，并且生物标志物和耐药机制还没有被完全理解。所以，鉴于PARPi可以增强ICI的治疗效果，因此PARPi与ICI的结合正在成为无法从ICI单药治疗中受益的患者的替代选择。在这篇综述中，我们集中于PARPi的机制和免疫作用，并讨论了该联合疗法的原理和临床研究。