期刊
CELL
卷 175, 期 2, 页码 313-326出版社
CELL PRESS
DOI: 10.1016/j.cell.2018.09.035
关键词
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资金
- US NIH [P50 CA196530, P30 CA16359]
- Yale University endowed chair from the United Technologies Corporation
- Miguel Servet contract from Instituto de Salud Carlos III, Fondo de Investigacion Sanitaria (Spain)
Harnessing an antitumor immune response has been a fundamental strategy in cancer immunotherapy. For over a century, efforts have primarily focused on amplifying immune activation mechanisms that are employed by humans to eliminate invaders such as viruses and bacteria. This immune enhancement'' strategy often results in rare objective responses and frequent immune-related adverse events (irAEs). However, in the last decade, cancer immunotherapies targeting the B7-H1/PD-1 pathway (anti-PD therapy), have achieved higher objective response rates in patients with much fewer irAEs. This more beneficial tumor response-to-toxicity profile stems from distinct mechanisms of action that restore tumor-induced immune deficiency selectively in the tumor microenvironment, here termed (i)mmune normalization,'' which has led to its FDA approval in more than 10 cancer indications and facilitated its combination with different therapies. In this article, we wish to highlight the principles of immune normalization and learn from it, with the ultimate goal to guide better designs for future cancer immunotherapies.
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