期刊
JOURNAL OF EXPERIMENTAL MEDICINE
卷 216, 期 12, 页码 2854-2868出版社
ROCKEFELLER UNIV PRESS
DOI: 10.1084/jem.20190801
关键词
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资金
- National Cancer Institute of the National Institutes of Health [P30 CA016359]
- Yale Cancer Center Innovation Award
- National Cancer Institute/National Institutes of Health [F30CA236466]
- Yale University Blavatnik Innovation Award
Cytosolic nucleic acid-sensing pathways can be triggered to enhance immune response to cancer. In this study, we tested the antitumor activity of a unique RIG-I agonist, stem loop RNA (SLR) 14. In the immunogenic tumor models, we observed significant tumor growth delay and an extended survival in SLR14-treated mice. SLR14 also greatly improved antitumor efficacy of anti-PD1 antibody over single-agent treatment. SLR14 was mainly taken up by CD11b(+) myeloid cells in the tumor microenvironment, and many genes associated with immune defense were significantly up-regulated after treatment, accompanied by increase in the number of CD8(+ )T lymphocytes, NK cells, and CD11b(+) cells in SLR14-treated tumors. Strikingly, SLR14 dramatically inhibited nonimmunogenic B16 tumor growth, and the cured mice developed an immune memory. Furthermore, a systemic antitumor response was observed in both bilateral and tumor metastasis models. Collectively, our results demonstrate that SLR14 is a promising therapeutic RIG-I agonist for cancer treatment, either alone or in combination with existing immunotherapies.
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