title: Pathogenesis of autoimmune hepatitis.
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 naïve 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.
authors: Institute of Liver Studies, King's College London School of Medicine at King's College Hospital, Denmark Hill, London SE5 9RS, UK.
authors: Rodrigo
authors: R
authors: Liberal
authors: Maria Serena
authors: MS
authors: Longhi
authors: Giorgina
authors: G
authors: Mieli-Vergani
authors: Diego
authors: D
authors: Vergani
mesh_terms: D000818:Animals; D004195:Disease Models, Animal; D019693:Hepatitis, Autoimmune / Q000235:genetics* / Q000276:immunology*; D006801:Humans; D007111:Immunity, Cellular; D056724:Immunity, Humoral; D051379:Mice; D006377:T-Lymphocytes, Helper-Inducer; D050378:T-Lymphocytes, Regulatory