Metabolic regulation of hepatitis B immunopathology by myeloid-derived suppressor cells View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2015-06

AUTHORS

Laura J Pallett, Upkar S Gill, Alberto Quaglia, Linda V Sinclair, Maria Jover-Cobos, Anna Schurich, Kasha P Singh, Niclas Thomas, Abhishek Das, Antony Chen, Giuseppe Fusai, Antonio Bertoletti, Doreen A Cantrell, Patrick T Kennedy, Nathan A Davies, Muzlifah Haniffa, Mala K Maini

ABSTRACT

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. More... »

PAGES

591-600

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/nm.3856

DOI

http://dx.doi.org/10.1038/nm.3856

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1039659443

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/25962123


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