Historically, breast cancer tumors have been considered immunologically quiescent, with the majority of tumors demonstrating low lymphocyte infiltration, low mutational burden, and modest objective response rates to anti-PD-1/PD-L1 monotherapy. Tumor and immunologic profiling has shed light on potential mechanisms of immune evasion in breast cancer, as well as unique aspects of the tumor microenvironment (TME). These include elements associated with antigen processing and presentation as well as immunosuppressive elements, which may be targeted therapeutically. Examples of such therapeutic strategies include efforts to (1) expand effector T-cells, natural killer (NK) cells and immunostimulatory dendritic cells (DCs), (2) improve antigen presentation, and (3) decrease inhibitory cytokines, tumor-associated M2 macrophages, regulatory T- and B-cells and myeloid derived suppressor cells (MDSCs). The goal of these approaches is to alter the TME, thereby making breast tumors more responsive to immunotherapy. In this review, we summarize key developments in our understanding of antitumor immunity in breast cancer, as well as emerging therapeutic modalities that may leverage that understanding to overcome immunologic resistance.

从历史上看，乳腺癌肿瘤被认为是免疫静止的，大多数肿瘤表现出低淋巴细胞浸润、低突变负荷以及对抗 PD-1/PD-L1 单一疗法的客观反应率适中。肿瘤和免疫分析揭示了乳腺癌免疫逃避的潜在机制，以及肿瘤微环境 (TME) 的独特方面。这些包括与抗原加工和呈递相关的元件以及可以作为治疗目标的免疫抑制元件。此类治疗策略的例子包括 (1) 扩大效应 T 细胞、自然杀伤 (NK) 细胞和免疫刺激性树突状细胞 (DC)，(2) 改善抗原呈递，以及 (3) 减少抑制性细胞因子、肿瘤相关 M2巨噬细胞、调节性 T 细胞和 B 细胞以及骨髓源性抑制细胞 (MDSC)。这些方法的目标是改变 TME，从而使乳腺肿瘤对免疫治疗更敏感。在这篇综述中，我们总结了我们对乳腺癌抗肿瘤免疫理解的关键进展，以及可能利用这种理解来克服免疫抵抗的新兴治疗方式。