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Abstract
Autoimmune hepatitis (AIH) is characterized by a progressive destruction of the liver parenchyma and a chronic fibrosis. The current treatment of autoimmune hepatitis is still largely dependent on the administration of corticosteroids and cytostatic drugs. For a long time the development of novel therapeutic strategies has been hampered by a lack of understanding the basic immunopathogenic mechanisms of AIH and the absence of valid animal models. However, in the past decade, knowledge from clinical observations in AIH patients and the development of innovative animal models have led to a situation where critical factors driving the disease have been identified and alternative treatments are being evaluated. Here we will review the insight on the immunopathogenesis of AIH as gained from clinical observation and from animal models.
Highlights
Autoimmune hepatitis (AIH) is characterized by a progressive destruction of the liver parenchyma and a chronic fibrosis
Reviews on autoimmune hepatitis often contain statements that not much is known about the etiology of the disease and that the mechanisms of the hepatic damage have not been uncovered in detail
One has to acknowledge the progress that has been made in the past three decades from the discovery of chronic active hepatitis that was often associated with a dire long-term prognosis and the requirement of a liver transplant, to current therapeutic interventions that result in a favorable outcome for most patients
Summary
Autoimmune hepatitis (AIH) is a serious autoimmune liver disease that is characterized by a progressive destruction of the liver parenchyma and the development of chronic fibrosis [1,2,3,4,5]. AIH type 1 has been characterized by the presence of anti-nuclear (ANA) and/or anti-smooth muscle (SMA) autoantibodies, whereas type 1 liver/kidney microsomal autoantibodies (LKM-1) have been considered as the hallmark of AIH type 2 [3,9,21,26]. Recently, such a classification has been questioned since patients with type 1 and type 2 AIH share the same clinical phenotype [27]. CYP2D6-specific cluster of differentiation (CD) 4 and CD8 T cells were found in the blood and the liver of AIH patients [32,33]
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