期刊
BEST PRACTICE & RESEARCH CLINICAL GASTROENTEROLOGY
卷 25, 期 6, 页码 653-664出版社
ELSEVIER SCI LTD
DOI: 10.1016/j.bpg.2011.09.009
关键词
Liver; Immune-regulation; Humoural immunity; Cellular immunity
资金
- Fundacao para a Ciencia e Tecnologia, Portugal [SFRH/BD/65007/2009]
- Medical Research Council, UK
- WellChild, Cheltenham
- Children's Liver Disease Foundation, Birmingham, UK
- Roger Dobson Fund
- Associazione Malattie Epatiche Autoimmuni (AMEA)
- MRC [G0902288] Funding Source: UKRI
- Medical Research Council [G0902288] Funding Source: researchfish
- Fundação para a Ciência e a Tecnologia [SFRH/BD/65007/2009] Funding Source: FCT
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.
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