Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
3294135 | Gastroenterology | 2012 | 13 Pages |
Abstract
Interaction between HAV and its receptor HAVCR1 inhibits Treg-cell function, resulting in an immune imbalance that allows viral expansion with limited hepatocellular damage during early stages of infection-a characteristic of HAV pathogenesis. The mechanism by which HAV is cleared in the absence of Treg-cell function could be used as a model to develop anticancer therapies, modulate autoimmune and allergic responses, and prevent transplant rejection.
Keywords
TGF-βTregAP-1HAVIGVTCrHEKNFATPBMCPtdSermAbFOXP3PI3K/AKTMonoclonal antibodyinterleukinTransforming growth factor βViral clearanceTeffPeripheral blood mononuclear cellCD4+CD25+ regulatory T cellsNuclear Factor of Activated T CellsPhosphatidylserinepolymerase chain reactionPCRHAV, Hepatitis A virusactivator protein 1forkhead box protein 3human embryonic kidneyT-cell receptor
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Authors
Mohanraj Manangeeswaran, Jérôme Jacques, Cecilia Tami, Krishnamurthy Konduru, Nadia Amharref, Oreste Perrella, Jose M. Casasnovas, Dale T. Umetsu, Rosemarie H. DeKruyff, Gordon J. Freeman, Alessandro Perrella, Gerardo G. Kaplan,