Energy metabolism drives myeloid-derived suppressor cell differentiation and functions in pathology. Issue 2 (21st February 2017)

• Record Type: Journal Article
• Authors: Sica, Antonio; Strauss, Laura
• Is Part Of: Journal of leukocyte biology. Volume 102:Issue 2(2017)
• Page Start: 325
• Page End: 334
• Publication Date: 2017-02-21
• Subjects: myeloid cell metabolism -- emergency myelopoiesis -- myeloid suppressor cells -- lipid metabolism -- cancer cachexia; Leucocytes -- Periodicals; Reticulo-endothelial system -- Periodicals; 571.96
• DOI: 10.1189/jlb.4MR1116-476R
• Languages: English
• ISSNs: 0741-5400

Abstract

Abstract : Review on the functional relationship between cell metabolism and differentiation of myeloid suppressor cells, highlighting the importance in cancer and inflammatory and metabolic chronic diseases. Abstract: Over the last decade, a heterogeneous population of immature myeloid cells with major regulatory functions has been described in cancer and other pathologic conditions and ultimately defined as MDSCs. Most of the early work on the origins and functions of MDSCs has been in murine and human tumor bearers in which MDSCs are known to be immunosuppressive and to result in both reduced immune surveillance and antitumor cytotoxicity. More recent studies, however, suggest that expansion of these immature myeloid cells may be linked to most, if not all, chronic and acute inflammatory processes. The universal expansion to inflammatory stimuli of MDSCs suggests that these cells may be more of a normal component of the inflammatory response (emergency myelopoiesis) than simply a pathologic response to a growing tumor. Instead of an adverse immunosuppressive response, expansion of these immature myeloid cell populations may result from a complex balance between increased immune surveillance and dampened adaptive immune responses that are common to many inflammatory responses. Within this scenario, new pathways of metabolic reprogramming are emerging as drivers of MDSC differentiation and functions in cancer and inflammatory disorders, crucially linking metabolic syndrome to inflammatory processes.