- 现金
- 6875 元
- 精华
- 8
- 帖子
- 977
- 注册时间
- 2006-10-2
- 最后登录
- 2024-5-28
|
http://www.nature.com/nm/journal/v21/n6/abs/nm.3856.html
【标题】:Metabolic regulation of hepatitis B immunopathology by myeloid-derived suppressor cells
【作者】:Pallett, L. J.; Gill, U. S.; Quaglia, A. (...)
【来源】:Nat Med, 2015, 21(6), 591-600
【摘要】:Infection with hepatitis B virus (HBV) results in disparate degrees of tissue injury: the virus can either replicate without pathological consequences or trigger immune-mediated necroinflammatory liver damage. We investigated the potential for myeloid-derived suppressor cells (MDSCs) to suppress T cell-mediated immunopathology in this setting. Granulocytic MDSCs (gMDSCs) expanded transiently in acute resolving HBV, decreasing in frequency prior to peak hepatic injury. In persistent infection, arginase-expressing gMDSCs (and circulating arginase) increased most in disease phases characterized by HBV replication without immunopathology, whilst L-arginine decreased. gMDSCs expressed liver-homing chemokine receptors and accumulated in the liver, their expansion supported by hepatic stellate cells. We provide in vitro and ex vivo evidence that gMDSCs 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 gMDSCs to regulate liver immunopathology in HBV infection. |
-
总评分: 现金 + 1
查看全部评分
|