- 著者
-
塚原 富士子
丸 義朗
- 出版者
- 東京女子医科大学学会
- 雑誌
- 東京女子医科大学雑誌 (ISSN:00409022)
- 巻号頁・発行日
- vol.90, no.6, pp.119-125, 2020-12-25 (Released:2020-12-25)
- 参考文献数
- 30
Inflammation is a biological defense mechanism, and the immune system plays a central role in recognizing and eliminating external and internal pathogens. However, oxidative stress due to chronic inflammation accumulates DNA mutations and increases the risk of cancer. The immune system can recognize and eliminate immunogenic cancer cells. Inflammation-related molecules, including cytokines and chemokines, not only promote the malignant transformation, but also accumulate immunosuppressive cells, such as M2-like tumor-associated macrophages and myeloid-derived suppressor cells, in the tumor microenvironment. Tumor cells escape immune attack by placing brakes on the immune cell responses. Immune checkpoint inhibitors activate the immune system by releasing the brake. Although immune checkpoint inhibitors have demonstrated significant therapeutic effects in intractable cancers, the therapeutic effects are limited and overcoming drug resistance is a problem. In order to overcome drug resistance, combined immunotherapy, comprising immune checkpoint inhibitors, angiogenesis inhibitors, and chemotherapeutic agents, is required. In this review, we have outlined the relationship between inflammation and cancer, the roles of cytokines, chemokines, immunosuppressive cells, and current progress in using immune checkpoint inhibitors as a therapeutic.