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

There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

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 RORγt 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 RORγt and Foxp3 and can play an important role in the treatment of AIH.

Related collections

Most cited references 33

Record: found
Abstract: found
Article: not found

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

Michael Ehrenstein, Jamie G. Evans, Animesh Singh … (2004)

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.

0 comments Cited 256 times – based on 0 reviews      Review now

Bookmark

Record: found
Abstract: not found
Article: not found

Autoimmune hepatitis.

Edward L Krawitt (2006)

0 comments Cited 192 times – based on 0 reviews      Review now

Bookmark

Record: found
Abstract: found
Article: not found

The Th17/Treg imbalance in patients with acute coronary syndrome.

Jiao Xie, Qing Fu, Yu Liao … (2008)

Atherosclerosis is a chronic inflammatory disease regulated by T lymphocyte subsets. Recently, CD4+CD25+Foxp3+ regulatory T (Treg) cells and Th17 cells have been described as two distinct subsets from Th1 and Th2 cells and have the opposite effects on autoimmunity. Th17/Treg balance controls inflammation and may be important in the pathogenesis of plaque destabilization and the onset of acute coronary syndrome [ACS, including unstable angina (UA) and acute myocardial infarction (AMI)]. To assess whether this balance was broken in patients with coronary heart disease, we detected Th17/Treg functions on different levels including cell frequencies, related cytokine secretion and key transcription factors in patients with AMI, UA, stable angina (SA) and controls. The results demonstrated that patients with ACS revealed significant increase in peripheral Th17 number, Th17 related cytokines (IL-17, IL-6 and IL-23) and transcription factor (RORgammat) levels and obvious decrease in Treg number, Treg related cytokines (IL-10 and TGF-beta1) and transcription factor (Foxp3) levels as compared with patients with SA and controls. Results indicate that Th17/Treg functional imbalance exists in patients with ACS, suggesting a potential role for Th17/Treg imbalance in plaque destabilization and the onset of ACS.