Pathogenesis of autoimmune hepatitis

TY - JOUR

T1 - Pathogenesis of autoimmune hepatitis

AU - Liberal, Rodrigo

AU - Longhi, Maria Serena

AU - Mieli-Vergani, Giorgina

AU - Vergani, Diego

PY - 2011/12

Y1 - 2011/12

N2 - 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.

AB - 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.

U2 - 10.1016/j.bpg.2011.09.009

DO - 10.1016/j.bpg.2011.09.009

M3 - Article

VL - 25

SP - 653

EP - 664

JO - BEST PRACTICE AND RESEARCH CLINICAL GASTROENTEROLOGY

JF - BEST PRACTICE AND RESEARCH CLINICAL GASTROENTEROLOGY

IS - 6

ER -