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Pratima Sinha

Researcher at University of Maryland, Baltimore County

Publications -  41
Citations -  9673

Pratima Sinha is an academic researcher from University of Maryland, Baltimore County. The author has contributed to research in topics: Myeloid-derived Suppressor Cell & Immune system. The author has an hindex of 28, co-authored 41 publications receiving 8736 citations. Previous affiliations of Pratima Sinha include University of Maryland, Baltimore.

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Journal ArticleDOI

Myeloid-Derived Suppressor Cells: Linking Inflammation and Cancer

TL;DR: The characterization and suppressive mechanisms used by myeloid-derived suppressor cells to block tumor immunity are reviewed and the mechanisms by which inflammation promotes tumor progression through the induction of MDSC are described.
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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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Proinflammatory S100 proteins regulate the accumulation of myeloid-derived suppressor cells.

TL;DR: It is shown that this population of immature myeloid cells induced by a given tumor share a common phenotype regardless of their in vivo location, and that Gr1highCD11bhighF4/80−CD80+IL4Rα+/−Arginase+ MDSC are induced by the proinflammatory proteins S100A8/A9.