NDLI: Foxp3 Expression in Liver Correlates with the Degree but Not the Cause of Inflammation

Content Provider	PubMed Central
Author	Speletas, Matthaios Argentou, Nikoletta Georgios, Germanidis Vasiliadis, Themistoclis Konstantinos, Mantzoukis Patsiaoura, Kalliopi Nikolaidis, Pavlos Karanikas, Vaios Konstantinos, Ritis Germenis, Anastasios E.
Copyright Year	2011
Abstract	Patients with chronic viral hepatitis display increased expression of Foxp3 in liver, suggesting that Tregs expansion contributes to persistent infection. The purpose of this study was to elucidate whether the expression of Foxp3 relates not to the viral infection but to the resulting liver inflammation. Liver biopsies obtained from 69 individuals (26 chronic HBV hepatitis, 14 chronic HCV hepatitis, 11 nonalcoholic fatty liver disease, 8 autoimmune diseases, 2 methotrexate-related toxicity, and 8 controls) were examined, by qRT-PCR, for the mRNA expression of Foxp3, IL-10, TGF-β1, Fas, FasL, TRAIL, caspase-3, TNF-α, IFN-γ, and IL-1β . Significant increase of Foxp3 was observed in all disease groups compared to controls, which was positively correlated with the intensity of inflammation. The expression of the apoptosis mediators Fas, FasL, and TRAIL, but not of IL-10 and TGF-β1, was also significantly elevated. Our findings indicate that, independently of the initial inducer, liver inflammation is correlated with elevated expression of apoptosis mediators and is followed by local Treg accumulation. Further research towards the elucidation of the underlying casual relationships is required, in order to clarify whether our results signify the existence of a uniform Treg-mediated regulatory mechanism of apoptosis-induced inflammation.
Related Links	http://dx.doi.org/10.1155/2011/827565
Starting Page	827565
File Format	PDF
ISSN	09629351
e-ISSN	14661861
Journal	Mediators of Inflammation
Volume Number	2011
Language	English
Publisher	Hindawi Publishing Corporation
Publisher Date	2011-01-01
Access Restriction	Open
Rights Holder	Hindawi Publishing Corporation
Subject Keyword	Immunology Cell Biology Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Cell Biology Immunology

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