Molecular mechanisms regulating myeloid-derived suppressor cell differentiation and function
By T. Condamine, D. Gabrilovich. Trends in immunology, 2010
858 citations recorded by the source corpus.
Myeloid derived suppressor cells (MDSCs) are one of the main cell populations responsible for regulating immune responses. MDSCs accumulate during tumor progression, autoimmunity, chronic infection and other pathological conditions and can potently suppress T cell function. Recent studies have demonstrated the ability of MDSCs to modulate the activity of NK and myeloid cells and have implicated MDSCs in the induction of regulatory T cells. In this review we discuss recent findings that describe the molecular mechanisms that regulate expansion and function of MDSCs, as well as recent attempts to use MDSCs in cell therapy for different pathologic conditions.
Subfields: Immunology
View Paper: https://www.semanticscholar.org/paper/43e1719f0e2b82247ba75014491577ed2fc89710
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In Immunology
Citations in the corpus
- Tumor-Derived Lactate Modifies Antitumor Immune Response: Effect on Myeloid-Derived Suppressor Cells and NK Cells (2013, background): “A “two-signal” model (34) suggests that two separate signaling pathways regulate MDSC accumulation: a first step that is promoted by chronic inflammation involves factors including GM-CSF and IL-6 and signals via STAT3 and STAT5 and promotes proliferation of immature myeloid cells.”
- A Comprehensive Review and Update on the Pathogenesis of Inflammatory Bowel Disease (2019, background): “MDSC suppress immunity by perturbing both innate and adaptive immune responses through secreted soluble mediators and induction of Treg cell expansion [74, 76].”
- Myeloid-derived suppressor cells in the tumor microenvironment: expect the unexpected. (2015, background): “We previously suggested that accumulation of bona fide MDSCs requires two sets of signals (53).”
- Dual Roles of Immune Cells and Their Factors in Cancer Development and Progression (2011, background): “oxide, reactive oxygen species and TGF-β secretion while also promoting Treg induction and favoring anti-inflammatory responses (19, 20).”