Abstract
(0.89±0.52%) versus blood (0.05±0.01%; p =0.0005) and their numbers correlated with advanced stages of fibrosis (p = 0.022), but not to inflammation. Finally, in vitro supernatants of Tregs induced mRNA up-regulation of profibrogenic markers TIMP1, MMP2, TGFbeta1 and alpha-SMA in resting HSC (p < 0.05 each). Conclusion: Our data demonstrate that in chronic hepatitis C Foxp3CD4 Tregs are enriched in areas of hepatic fibrosis, exhibit up-regulated IL-8 expression and can activate HSC. Thus, in addition to suppression of inflammation adaptive Tregs in hepatitis C play a dual role as regulators of fibrogenesis.
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