Journal
ONCOIMMUNOLOGY
Volume 6, Issue 6, Pages -Publisher
TAYLOR & FRANCIS INC
DOI: 10.1080/2162402X.2017.1320011
Keywords
CD39; CD73; MDSCs; NSCLC; TGF-
Categories
Funding
- National Institutes of Health [CA149669, CA208354]
- National Natural Science Foundation of China [81171985, 81171986]
- Ministry of Public Health [20110110001]
- Basic and Advanced Technology Research Foundation from Science and Technology Department of Henan Province [112300410153, 122300410155]
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CD39/CD73-adenosine pathway has been recently defined as an important tumor-induced immunosuppressive mechanism. We here documented a fraction of CD11b(+)CD33(+) myeloid-derived suppressor cells (MDSCs) in peripheral blood and tumor tissues from non-small cell lung cancer (NSCLC) patients expressed surface ectonucleotidases CD39 and CD73. Tumor TGF- stimulated CD39 and CD73 expression, thereby inhibited T cell and NK cell activity, and protected tumor cells from the cytotoxic effect of chemotherapy through ectonucleotidase activity. Mechanistically, TGF- triggered phosphorylation of mammalian target of rapamycin, and subsequently activated hypoxia-inducible factor-1 (HIF-1) that induced CD39/CD73 expression on MDSCs. CD39 and CD73 on MDSCs, therefore, link their immunosuppressive and chemo-protective effects to NSCLC progression, providing novel targets for chemo-immunotherapeutic intervention.
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