Wang Dingzhi, DuBois Raymond N
Laboratory for Inflammation and Cancer, The Biodesign Institute and.
Laboratory for Inflammation and Cancer, The Biodesign Institute and Department of Chemistry and Biochemistry, Arizona State University, PO Box 875001, 1001 S. McAllister Ave., Tempe, AZ 85287, USA and Department of Research and Division of Gastroenterology, Mayo Clinic, Scottsdale, AZ 85259, USA
Carcinogenesis. 2015 Oct;36(10):1085-93. doi: 10.1093/carcin/bgv123. Epub 2015 Sep 8.
Chronic inflammation contributes to cancer development via multiple mechanisms. One potential mechanism is that chronic inflammation can generate an immunosuppressive microenvironment that allows advantages for tumor formation and progression. The immunosuppressive environment in certain chronic inflammatory diseases and solid cancers is characterized by accumulation of proinflammatory mediators, infiltration of immune suppressor cells and activation of immune checkpoint pathways in effector T cells. In this review, we highlight recent advances in our understanding of how immunosuppression contributes to cancer and how proinflammatory mediators induce the immunosuppressive microenvironment via induction of immunosuppressive cells and activation of immune checkpoint pathways.
慢性炎症通过多种机制促进癌症发展。一种潜在机制是慢性炎症可产生免疫抑制微环境,为肿瘤形成和进展提供有利条件。某些慢性炎症性疾病和实体癌中的免疫抑制环境的特征是促炎介质的积累、免疫抑制细胞的浸润以及效应T细胞中免疫检查点通路的激活。在本综述中,我们重点介绍了我们在理解免疫抑制如何促进癌症以及促炎介质如何通过诱导免疫抑制细胞和激活免疫检查点通路来诱导免疫抑制微环境方面的最新进展。