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Deprecated: Implicit conversion from float 263.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Immunity 2014 ; 41 (6): 947-59 Nephropedia Template TP
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Myeloid-derived suppressor activity is mediated by monocytic lineages maintained by continuous inhibition of extrinsic and intrinsic death pathways #MMPMID25500368
Haverkamp JM; Smith AM; Weinlich R; Dillon CP; Qualls JE; Neale G; Koss B; Kim Y; Bronte V; Herold MJ; Green DR; Opferman JT; Murray PJ
Immunity 2014[Dec]; 41 (6): 947-59 PMID25500368show ga
Non-resolving inflammation expands a heterogeneous population of myeloid suppressor cells capable of inhibiting T cell function. This heterogeneity has confounded the functional dissection of individual myeloid subpopulations and presents an obstacle for anti-tumor immunity and immunotherapy. Using genetic manipulation of cell death pathways, we found the monocytic suppressor cell subset, but not the granulocytic subset requires continuous c-FLIP expression to prevent caspase-8-dependent, RIPK3-independent cell death. Development of the granulocyte subset requires MCL-1-mediated control of the intrinsic mitochondrial death pathway. Monocytic suppressors tolerate the absence of MCL-1 provided cytokines increase expression of the MCL-1-related protein A1. Monocytic suppressors mediate T cell suppression, while their granulocytic counterparts lack suppressive function. The loss of the granulocytic subset via conditional MCL-1 deletion did not alter tumor incidence implicating the monocytic compartment as the functionally immunosuppressive subset in vivo. Thus, death pathway modulation defines the development, survival and function of myeloid suppressor cells.