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Abstract Autoimmune hepatitis (AIH) which was first described in 1950 by Waldenstrom as a chronic form of hepatitis in young women and in 1965 it became designated by Mackay et al. as ”Autoimmune Hepatitis represents one of the most important causes of chronic liver diseases in children. It is generally progressive, chronic inflammatory disease of the liver with fluctuating activity that occurs worldwide in children and adults. The pathogenesis of AIH postulates an environmental agent that triggers a cascade of T-cellmediated events directed at liver antigens in a host genetically predisposed to this disease, leading to a progressive necroinflammatory and fibrotic process in the liver. T helper17 cells are a newly detected subset of T-helper cells which produced from naive CD4+ T cell in presence of IL-6 in combination with TGF-â. T helper17 cells can produce multiple cytokines including IL-17A IL-17F, IL-21 and IL-22. IL-17 is a potent proinflammatory cytokine that amplifies inflammation by inducing expression of tumor necrosis factor-á(TNF-á), IL-1â, and IL-6 in epithelial and endothelial cells as well as other cell types such as keratinocytes, synoviocytes, fibroblasts, and macrophages. In AIH IL-17 induce the production of IL-6 in the hepatocyte, which in turn leads to increase production of Th 17 cells (positive feedback loop between Th17 cells and hepatocytes) while leads to decrease the regulatory. |