期刊
SEMINARS IN IMMUNOLOGY
卷 60, 期 -, 页码 -出版社
ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
DOI: 10.1016/j.smim.2022.101642
关键词
Macrophage; Myeloid cell; Complement; Cancer; Cancer-related inflammation; Immunosuppression; Immunotherapy
类别
资金
- Fondazione Cariplo [2016-0568]
- Ministero della Salute [RF-2013-02355470]
- Ministero dell'Istruzione, dell'Universita e della Ricerca (MIUR) [PRIN 20174T7NXL]
- Associazione Italiana Ricerca sul Cancro(AIRC ) [21714, 21147]
Inflammation related to cancer plays a key role in promoting tumor development, and the complement system is one of the inflammatory mechanisms activated in the tumor microenvironment. It can affect tumor growth by promoting immunosuppression and invasiveness.
Cancer-related inflammation plays a central role in the establishment of tumor-promoting mechanisms. Tumor-associated myeloid cells, which engage in complex interactions with cancer cells, as well as stromal and tumor immune infiltrating cells, promote cancer cell proliferation and survival, angiogenesis, and the generation of an immunosuppressive microenvironment. The complement system is one of the inflammatory mechanisms activated in the tumor microenvironment. Beside exerting anti-tumor mechanisms such as complement-dependent cytotoxicity and phagocytosis induced by therapeutic monoclonal antibodies, the complement system may promote immunosuppression and tumor growth and invasiveness, in particular, through the anaphylatoxins which target both leukocytes and cancer cells. In this review, we will discuss complement-mediated mechanisms acting on leukocytes, in particular on cells of the myelomonocytic cell lineage (macrophages, neutrophils, myeloid derived suppressor cells), which promote myeloid cell recruitment and functional skewing, leading to immunosuppression and resistance to tumor-specific immunity. Pre-clinical studies, which have elucidated the role of complement in activating pro-tumor mechanisms in myeloid cells, showing the relevance of these mechanisms in human, and therapeutic approaches based on complement targeting support the hypothesis that complement directly and indirectly interferes with many of the effector pathways associated with the cancer-immunity cycle, suggesting the relevance of complement targeting to improve responses to immunotherapeutic approaches.
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