Pathogenesis of autoimmune hepatitis

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    Abstract

    The mechanisms underlying the pathogenesis of autoimmune hepatitis are not fully understood, though there is growing evidence that genetic predisposition, molecular mimicry and/or impairment of regulatory T-cells are involved in the initiation and perpetuation of the autoimmune liver attack. The histological picture of interface hepatitis, characterized by a dense portal mononuclear cell infiltrate, was the first to suggest an autoaggressive cellular immune attack in the pathogenesis of this condition. Liver damage is likely to be orchestrated by CD4(pos) T-cells recognizing an autoantigenic liver peptide. For autoimmunity to arise, the peptide must be presented by antigen-presenting cells to naive CD4(pos) T-helper (Th0) cells. Once activated, Th0-cells can differentiate into Th1-, Th2-, or Th17-cells, initiating a cascade of immune reactions that are determined by the cytokines they produce. Autoantigen recognition and the above effector mechanisms are opposed by regulatory T-cells, a cell subset numerically and functionally impaired in autoimmune hepatitis. (C) 2011 Elsevier Ltd. All rights reserved.
    Original languageEnglish
    Pages (from-to)653 - 664
    Number of pages12
    JournalBEST PRACTICE AND RESEARCH CLINICAL GASTROENTEROLOGY
    Volume25
    Issue number6
    DOIs
    Publication statusPublished - Dec 2011

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