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Virginia K. Clements

Researcher at University of Maryland, Baltimore County

Publications -  41
Citations -  6936

Virginia K. Clements is an academic researcher from University of Maryland, Baltimore County. The author has contributed to research in topics: Immune system & Myeloid-derived Suppressor Cell. The author has an hindex of 26, co-authored 41 publications receiving 6191 citations.

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Myeloid-derived suppressor cells inhibit T-cell activation by depleting cystine and cysteine.

TL;DR: It is shown that MDSCs also block T-cell activation by sequestering cystine and limiting the availability of cysteine, depriving T cells of the Cysteine they require for activation and function.
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Cross-talk between myeloid-derived suppressor cells and macrophages subverts tumor immunity toward a type 2 response.

TL;DR: MDSC impair tumor immunity by suppressing T cell activation and by interacting with macrophages to increase IL-10 and decrease IL-12 production, thereby promoting a tumor-promoting type 2 response, a process that can be partially reversed by gemcitabine.
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Prostaglandin E2 Promotes Tumor Progression by Inducing Myeloid-Derived Suppressor Cells

TL;DR: It is reported that host MDSC have receptors for prostaglandin E2 (PGE2) and that E-prostanoid receptor agonists, including PGE2, induce the differentiation of Gr1(+)CD11b(+) M DSC from bone marrow stem cells, whereas receptor antagonists block differentiation.
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Reduced Inflammation in the Tumor Microenvironment Delays the Accumulation of Myeloid-Derived Suppressor Cells and Limits Tumor Progression

TL;DR: Results show that immune suppression by MDSC and tumor growth are regulated by the inflammatory milieu and support the hypothesis that the induction of suppressor cells which down-regulate tumor immunity is one of the mechanisms linking inflammation and cancer.
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Inflammation Induces Myeloid-Derived Suppressor Cells that Facilitate Tumor Progression

TL;DR: It is suggested that inflammation promotes malignancy via proinflammatory cytokines, such as IL-1β, which enhance immune suppression through the induction of MSC, thereby counteracting immune surveillance and allowing the outgrowth and proliferation of malignant cells.