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Cited by 507

The DOI matches its Crossref record; 53 of the 53 references it cites were found in a registry or an index.

STAT3 regulates arginase-I in myeloid-derived suppressor cells from cancer patients

Open access
Vasquez-Dunddel, David, Pan, Fan, Zeng, Qi, Gorbounov, Mikhail, Albesiano, Emilia, Fu, Juan, Blosser, Richard L., Tam, Ada J., Bruno, Tullia, Zhang, Hao, Pardoll, Drew, Kim, Young·2013·Journal of Clinical Investigation

Abstract

Myeloid-derived suppressor cells (MDSC) play a key immunosuppressive role in various types of cancer, including head and neck squamous cell carcinoma (HNSCC). In this study, we characterized CD14+HLA-DR(-/lo) cells sorted from the tumors, draining lymph nodes, and peripheral blood of HNSCC patients. CD14+HLA-DR(-/lo) cells were phenotyped as CD11b+, CD33+, CD34+, arginase-I+, and ROS+. In all 3 compartments, they suppressed autologous, antigen-independent T cell proliferation in a differential manner. The abundance of MDSC correlated with stage, but did not correlate with previous treatment with radiation or subsites of HNSCC. Interestingly, MDSC from all 3 compartments showed high phosphorylated STAT3 levels that correlated with arginase-I expression levels and activity. Stattic, a STAT3-specific inhibitor, and STAT3-targeted siRNA abrogated MDSC’s suppressive function. Inhibition of STAT3 signaling also resulted in decreased arginase-I activity. Analysis of the human arginase-I promoter region showed multiple STAT3-binding elements, and ChIP demonstrated that phosphorylated STAT3 binds to multiple sites in the arginase-I promoter. Finally, rescue of arginase-I activity after STAT3 blockade restored MDSC’s suppressive function. Taken together, these results demonstrate that the suppressive function of arginase-I in both infiltrating and circulating MDSC is a downstream target of activated STAT3.

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Metadata

Authors
Vasquez-Dunddel, D., Pan, F., Zeng, Q., Gorbounov, M., Albesiano, E., Fu, J., Blosser, R. L., Tam, A. J., Bruno, T., Zhang, H., Pardoll, D., & Kim, Y.
Venue
Journal of Clinical Investigation
Published
2013-03-01
Volume
123
Issue
4
Pages
1580-1589
ISSN
0021-9738 (ISSN-L)
OpenAlex
W2046764077
Cited by
507
References
53
FWCI
21.08
Type
journal article
Language
en
Open access
hybrid

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CoChat. (2026). Citation check: STAT3 regulates arginase-I in myeloid-derived suppressor cells from cancer patients. https://app.cochat.ai/papers/10.1172/jci60083
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Vasquez-Dunddel, D., Pan, F., Zeng, Q., Gorbounov, M., Albesiano, E., Fu, J., Blosser, R. L., Tam, A. J., Bruno, T., Zhang, H., Pardoll, D., & Kim, Y. (2013). STAT3 regulates arginase-I in myeloid-derived suppressor cells from cancer patients. Journal of Clinical Investigation. https://doi.org/10.1172/jci60083

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

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