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      Chinese Medicine Bu Xu Hua Yu Recipe for the Regulation of Treg/Th17 Ratio Imbalance in Autoimmune Hepatitis

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          Abstract

          Objectives. The aim of this study is researching the role of the Regulatory T cell (Treg)/T helper cell-17 (Th17) cell ratio imbalance in the pathogenesis of autoimmune hepatitis (AIH) and the use of the “Bu Xu Hua Yu” recipe in the treatment of AIH. Materials and Methods. Sixty adult male C57/BL6 mice were divided into six different groups. α-Galcer was injected abdominally for production of the animal models. Liver function tests, histological examinations, liver tissue Regulatory T cell, and T helper cell-17 levels tests were carried out. TGF- β1, IL-10, IL-17, and expression of mRNA and protein levels of Foxp3 and ROR- γt were also assessed. Results. Bu Xu Hua Yu method increased the levels of Regulatory T cell, IL-10, and the expression of Foxp3 ( P < 0.05) in mice liver tissues. Furthermore, there were decreases in the levels of T helper cell-17, IL-17, and expression of ROR γt mRNA and protein ( P < 0.05). The ratio of Treg/Th17 was increased ( P < 0.05). Conclusion. Mice with AIH have a Treg/Th17 ratio imbalance. Bu Xu Hua Yu method was able to restore the cellular balance of Treg/Th17 through the regulation of the expression of ROR γt and Foxp3 and can play an important role in the treatment of AIH.

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          Most cited references 33

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          Compromised Function of Regulatory T Cells in Rheumatoid Arthritis and Reversal by Anti-TNFα Therapy

          Regulatory T cells have been clearly implicated in the control of disease in murine models of autoimmunity. The paucity of data regarding the role of these lymphocytes in human autoimmune disease has prompted us to examine their function in patients with rheumatoid arthritis (RA). Regulatory (CD4+CD25+) T cells isolated from patients with active RA displayed an anergic phenotype upon stimulation with anti-CD3 and anti-CD28 antibodies, and suppressed the proliferation of effector T cells in vitro. However, they were unable to suppress proinflammatory cytokine secretion from activated T cells and monocytes, or to convey a suppressive phenotype to effector CD4+CD25− T cells. Treatment with antitumor necrosis factor α (TNFα; Infliximab) restored the capacity of regulatory T cells to inhibit cytokine production and to convey a suppressive phenotype to “conventional” T cells. Furthermore, anti-TNFα treatment led to a significant rise in the number of peripheral blood regulatory T cells in RA patients responding to this treatment, which correlated with a reduction in C reactive protein. These data are the first to demonstrate that regulatory T cells are functionally compromised in RA, and indicate that modulation of regulatory T cells by anti-TNFα therapy may be a further mechanism by which this disease is ameliorated.
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            Autoimmune hepatitis.

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              An immunomodulatory role for CD4(+)CD25(+) regulatory T lymphocytes in hepatitis C virus infection.

              The CD4(+)CD25(+) regulatory T lymphocytes have been implicated in suppressing T cell immune responses. Our aim was to characterize the frequency, phenotype, function, and specificity of CD4(+)CD25(+) T cells in hepatitis C virus (HCV) infection. Peripheral CD4(+)CD25(+) cells from recovered (n = 15), chronic infected (n = 30), and normal control (n = 15) subjects were analyzed ex vivo for quantitation, phenotype, and effect on HCV-specific interferon gamma production and proliferation. CD4(+)CD25(+) specificity was determined by intracellular cytokine staining for interleukin 10 (IL-10). A higher proportion of CD4(+)CD25(+) were found in chronic infection (mean, 3.02%) when compared with recovered (1.64%, P = .001) and normal controls (2.27%, P = .02). CD4(+)CD25(+) cells display CD45RO(high), CD45RA(low), CD28(high), CD62L(high), and CD95(high) phenotype. HCV-specific interferon gamma activity was enhanced in peripheral blood mononuclear cells depleted of CD4(+)CD25(+) and suppressed in peripheral blood mononuclear cells enriched with CD4(+)CD25(+). Depletion of CD4(+)CD25(+) cells also enhanced HCV-specific CD4(+) and CD8(+) T cell proliferation. Cytokine analysis suggested CD4(+)CD25(+) cells secrete transforming growth factor beta (TGF-beta(1)) and IL-10. The inhibitory role for TGF-beta(1) was confirmed by anti-TGF-beta(1). Transwell studies showed CD4(+)CD25(+) mediated suppression to be dose dependent and requiring cell contact. CD4(+)CD25(+) cells showed HCV-specificity through IL-10 production, with a frequency ranging from 1.9% to 5.3%. A positive correlation was detected between CD4(+)CD25(+) T cell frequency and HCV RNA titer, whereas an inverse relation was found with liver inflammatory activity. In conclusion, CD4(+)CD25(+) T lymphocytes constitute a highly differentiated population and appear to play a role in viral persistence by suppressing HCV-specific T cell responses in a cell-cell contact manner.
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                Author and article information

                Journal
                Evid Based Complement Alternat Med
                Evid Based Complement Alternat Med
                ECAM
                Evidence-based Complementary and Alternative Medicine : eCAM
                Hindawi Publishing Corporation
                1741-427X
                1741-4288
                2015
                21 April 2015
                21 April 2015
                : 2015
                Affiliations
                1Department of Hepatology, Shanghai University of Traditional Chinese Medicine, Longhua Hospital, No. 725 South Wan Ping Road, Shanghai, China
                2Shanghai University of Traditional Chinese Medicine, Shuguang Hospital, Shanghai, China
                3Department of Gastroenterology, Renji Hospital, Shanghai Institute of Digestive Disease, Shanghai Jiao Tong University School of Medicine, China
                Author notes

                Academic Editor: Vincenzo De Feo

                Article
                10.1155/2015/461294
                4419233
                Copyright © 2015 Lei Wang et al.

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                Categories
                Research Article

                Complementary & Alternative medicine

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