Abstract

Objective To explore the differences of Th17 population and serum transforming growth factor(TGF)-β1 levels between early-and late-stage primary biliary cirrhosis(PBC) and their roles in pathogenesis. Methods Peripheral Th17 counts were analyzed by flow cytometry. The expression of IL-17A in peripheral blood mononuclear cells and TGF-β1 were measured by real-time quantitative polymerase chain reaction. Serum concentration of TGF-β1 was measured by enzyme-linked immunosorbent assay. Liver biopsies were stained with hematoxylin-eosin to determine the pathological stage. Results were evaluated using Krustal-Wallis test followed by Mann-WhitneyU tests for comparisons of Th17 population between patients with early and late PBC, patients with chronic hepatitis B(CHB) and health controls(HCs). ANOVA followed by LSDt-tests were used for comparing IL-17 mRNA, TGF-β1 mRNA and TGF-β1 serum concentration between groups. The correlations between Mayo risk score and peripheral Th17 of PBC patients, Mayo risk score and serum concentration of TGF-β1 was analyzed by Pearson correlation analysis separately. Results The peripheral Th17 population increased in patients with early PBC(1.03±0.33)%, compared to those with late PBC[(0.48±0.13%,U= 14.0,P<0.01], CHB [(0.56±0.35)%,U=104.5,P<0.01], and HCs [(0.36±0.17)%,U=8.0,P<0.01], while TGF-β1 changed in the opposite direction. Serum concentration of TGF-β1 elevated in late PBC(43.0±18.7) ng/ml compared with early PBC (29.5 ± 12.2) ng/ml,t=2.85,P=0.006. Conclusion The opposite changes of Th17 population and TGF-β1 level in early and late PBC indicated their different roles in different stages. Th17 may contribute to the autoimmune response in early PBC, participate in the occurrence of autoimmune inflammation, while TGF-β1 to fibrogenesis in late stage. In addition, the possible regulation mechanisms of differentiation of Th17 by TGF-β1 cannot be ignored. Key words: Livercirrhosis, biliary; T helper 17 cells; Transforming growth factor β1

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