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10.1111/j.1600-6143.2009.02757.x

http://scihub22266oqcxt.onion/10.1111/j.1600-6143.2009.02757.x
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19681826!ä!19681826

suck abstract from ncbi


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pmid19681826      Am+J+Transplant 2009 ; 9 (9): 2034-47
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  • Endotoxin-induced myeloid-derived suppressor cells inhibit alloimmune responses via heme oxygenase-1 #MMPMID19681826
  • De Wilde V; Van Rompaey N; Hill M; Lebrun JF; Lemaitre P; Lhomme F; Kubjak C; Vokaer B; Oldenhove G; Charbonnier LM; Cuturi MC; Goldman M; Le Moine A
  • Am J Transplant 2009[Sep]; 9 (9): 2034-47 PMID19681826show ga
  • Inflammation and cancer are associated with impairment of T-cell responses by a heterogeneous population of myeloid-derived suppressor cells (MDSCs) coexpressing CD11b and GR-1 antigens. MDSCs have been recently implicated in costimulation blockade-induced transplantation tolerance in rats, which was under the control of inducible NO synthase (iNOS). Herein, we describe CD11b+GR-1+MDSC-compatible cells appearing after repetitive injections of lipopolysaccharide (LPS) using a unique mechanism of suppression. These cells suppressed T-cell proliferation and Th1 and Th2 cytokine production in both mixed lymphocyte reaction and polyclonal stimulation assays. Transfer of CD11b+ cells from LPS-treated mice in untreated recipients significantly prolonged skin allograft survival. They produced large amounts of IL-10 and expressed heme oxygenase-1 (HO-1), a stress-responsive enzyme endowed with immunoregulatory and cytoprotective properties not previously associated with MDSC activity. HO-1 inhibition by the specific inhibitor, SnPP, completely abolished T-cell suppression and IL-10 production. In contrast, neither iNOS nor arginase 1 inhibition did affect suppression. Importantly, HO-1 inhibition before CD11b+ cell transfer prevented the delay of allograft rejection revealing a new MDSC-associated suppressor mechanism relevant for transplantation.
  • |Animals[MESH]
  • |CD11b Antigen/biosynthesis[MESH]
  • |Cell Proliferation[MESH]
  • |Endotoxins/*metabolism[MESH]
  • |Heme Oxygenase-1/*metabolism[MESH]
  • |Immune System[MESH]
  • |Interleukin-10/metabolism[MESH]
  • |Lipopolysaccharides/metabolism[MESH]
  • |Mice[MESH]
  • |Mice, Inbred BALB C[MESH]
  • |Mice, Inbred C57BL[MESH]
  • |Myeloid Cells/*cytology[MESH]
  • |Receptors, Chemokine/biosynthesis/immunology[MESH]
  • |T-Lymphocytes/cytology[MESH]
  • |Th1 Cells/cytology[MESH]


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