Complementing the Cancer-Immunity Cycle

癌症免疫疗法 免疫检查点 免疫学 免疫系统 细胞毒性T细胞 癌症 免疫疗法 背景(考古学) 癌症研究 T细胞 免疫 生物 医学 体外 古生物学 生物化学 遗传学
作者
Rubén Pı́o,Daniel Ajona,Sergio Ortiz‐Espinosa,Alberto Mantovani,John D. Lambris
出处
期刊:Frontiers in Immunology [Frontiers Media SA]
卷期号:10 被引量:152
标识
DOI:10.3389/fimmu.2019.00774
摘要

Reactivation of cytotoxic CD8+ T-cell responses has set a new direction for cancer immunotherapy. Neutralizing antibodies targeting immune checkpoint programmed cell death protein 1 (PD-1) or its ligand (PD-L1) have been particularly successful for tumor types with limited therapeutic options such as melanoma and lung cancer. However, reactivation of T cells is only one step toward tumor elimination, and a substantial fraction of patients fails to respond to these therapies. In this context, combination therapies targeting more than one of the steps of the cancer-immune cycle may provide substantial benefits. To find the best combinations, it is of upmost importance to understand the interplay between cancer cells and all the components of the immune response. This review focuses on the elements of the complement system that come into play in the cancer-immunity cycle. The complement system, an essential part of innate immunity, has emerged as a major regulator of cancer immunity. Complement effectors such as C1q, anaphylatoxins C3a and C5a, and their receptors C3aR and C5aR1 have been associated with tolerogenic cell death and inhibition of antitumor T-cell responses through the recruitment and/or activation of immunosuppressive cell subpopulations such as myeloid-derived suppressor cells (MDSCs), regulatory T cells (Tregs) or M2 tumor-associated macrophages (TAMs). Evidence is provided to support the idea that complement inhibition blocks many of the effector routes associated with the cancer-immunity cycle, providing the rationale for new therapeutic combinations aimed to enhance the antitumor efficacy of anti-PD-1/PD-L1 checkpoint inhibitors.

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