The DOI matches its Crossref record; 10 of the 10 references it cites were found in a registry or an index.
Myeloid-Derived Suppressor Cells: Linking Inflammation and Cancer
Open accessAbstract
Many cancer immunotherapies developed in experimental animals have been tested in clinical trials. Although some have shown modest clinical effects, most have not been effective. Recent studies have identified myeloid-origin cells that are potent suppressors of tumor immunity and therefore a significant impediment to cancer immunotherapy. “Myeloid-derived suppressor cells” (MDSC) accumulate in the blood, lymph nodes, and bone marrow and at tumor sites in most patients and experimental animals with cancer and inhibit both adaptive and innate immunity. MDSC are induced by tumor-secreted and host-secreted factors, many of which are proinflammatory molecules. The induction of MDSC by proinflammatory mediators led to the hypothesis that inflammation promotes the accumulation of MDSC that down-regulate immune surveillance and antitumor immunity, thereby facilitating tumor growth. This article reviews the characterization and suppressive mechanisms used by MDSC to block tumor immunity and describes the mechanisms by which inflammation promotes tumor progression through the induction of MDSC.
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Cites
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Self-citationThe JAK/STAT signaling pathway: from bench to clinic
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Metadata
- Authors
- Ostrand-Rosenberg, S., & Sinha, P.
- Venue
- The Journal of Immunology
- Publisher
- Oxford University Press (OUP)
- Published
- 2009-04
- Volume
- 182
- Issue
- 8
- Pages
- 4499-4506
- ISSN
- 0022-1767 (ISSN-L)
- 1550-6606
- OpenAlex
- W2157269800
- Cited by
- 1,736
- References
- 10
- FWCI
- 48.62
- Type
- journal article
- Language
- en
- Open access
- bronze
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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
