Ceci Claudia, Atzori Maria Grazia, Lacal Pedro Miguel, Graziani Grazia
Department of Systems Medicine, University of Rome Tor Vergata, Via Montpellier 1, 00133 Rome, Italy.
IDI-IRCCS, Via dei Monti di Creta 104, 00167 Rome, Italy.
Cancers (Basel). 2020 Nov 17;12(11):3401. doi: 10.3390/cancers12113401.
Immune checkpoint inhibitors (ICIs) represent a promising therapeutic intervention for a variety of advanced/metastatic solid tumors, including melanoma, but in a large number of cases, patients fail to establish a sustained anti-tumor immunity and to achieve a long-lasting clinical benefit. Cells of the tumor micro-environment such as tumor-associated M2 macrophages (M2-TAMs) have been reported to limit the efficacy of immunotherapy, promoting tumor immune evasion and progression. Thus, strategies targeting M2-TAMs have been suggested to synergize with immune checkpoint blockade. This review recapitulates the molecular mechanisms by which M2-TAMs promote cancer immune evasion, with focus on the potential cross-talk between pharmacological interventions targeting M2-TAMs and ICIs for melanoma treatment.
免疫检查点抑制剂(ICIs)是治疗多种晚期/转移性实体瘤(包括黑色素瘤)的一种有前景的治疗手段,但在大量病例中,患者无法建立持续的抗肿瘤免疫,也无法获得持久的临床益处。据报道,肿瘤微环境中的细胞,如肿瘤相关M2巨噬细胞(M2-TAMs),会限制免疫治疗的疗效,促进肿瘤免疫逃逸和进展。因此,有人提出靶向M2-TAMs的策略可与免疫检查点阻断协同作用。本综述概述了M2-TAMs促进癌症免疫逃逸的分子机制,重点关注靶向M2-TAMs的药物干预与用于黑色素瘤治疗的ICIs之间潜在的相互作用。