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Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Nat+Med 2015 ; 21 (6): 591-600 Nephropedia Template TP
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Metabolic regulation of hepatitis B immunopathology by myeloid-derived suppressor cells #MMPMID25962123
Pallett LJ; Gill US; Quaglia A; Sinclair LV; Jover-Cobos M; Schurich A; Singh KP; Thomas N; Das A; Chen A; Fusai G; Bertoletti A; Cantrell DA; Kennedy PT; Davies NA; Haniffa M; Maini MK
Nat Med 2015[Jun]; 21 (6): 591-600 PMID25962123show ga
Infection with hepatitis B virus (HBV) results in disparate degrees of tissue injury: it can replicate without pathological consequences or trigger immune-mediated necroinflammatory liver damage. We investigated the potential for myeloid-derived suppressor cells (MDSC) to suppress T cell-mediated immunopathology in this setting. Granulocytic MDSC (gMDSC) expanded transiently in acute resolving HBV, decreasing before peak hepatic injury. In persistent infection, arginase-expressing gMDSC (and circulating arginase) increased most in phases characterized by HBV replication without immunopathology, whilst L-arginine decreased. gMDSC expressed liver-homing chemokine receptors and accumulated in the liver, their expansion being supported by hepatic stellate cells. We provide in vitro and ex vivo evidence that gMDSC potently inhibited T cells in a partially arginase-dependent manner. L-arginine-deprived T cells upregulated system-L amino acid transporters to increase uptake of essential nutrients and attempt metabolic reprogramming. These data demonstrate the capacity of expanded arginase-expressing gMDSC to regulate liver immunopathology in HBV infection.