PMID- 20460892
OWN - NLM
STAT- MEDLINE
DCOM- 20100910
LR  - 20100512
IS  - 1421-9875 (Electronic)
IS  - 0257-2753 (Linking)
VI  - 28
IP  - 1
DP  - 2010
TI  - Adaptive immunity in autoimmune hepatitis.
PG  - 63-9
LID - 10.1159/000282066 [doi]
AB  - The histological lesion of interface hepatitis, with its dense portal cell 
      infiltrate consisting of lymphocytes, monocytes/macrophages and plasma cells, was 
      the first to suggest an autoaggressive cellular immune attack in the pathogenesis 
      of autoimmune hepatitis (AIH). Immunohistochemical studies, focused on the 
      phenotype of inflammatory cells infiltrating the liver parenchyma, have shown a 
      predominance of alphabeta-T cells. Amongst these cells, the majority have been 
      CD4 helper/inducers, while a sizeable minority have consisted of CD8 
      cytotoxic/suppressors. Lymphocytes on non-T cell lineage included natural killer 
      cells, monocytes/macrophages and B lymphocytes. For autoimmunity to arise, the 
      self-antigenic peptide, embraced by an human leukocyte antigen (HLA) class II 
      molecule, must be presented to an uncommitted T helper (T(H)0) lymphocyte by 
      professional antigen-presenting cells. Once activated and according to the 
      presence in the milieu of interleukin 12 (IL-12) or IL-4, T(H)0 lymphocytes can 
      differentiate into T(H)1 cells, which are pivotal to macrophage activation; 
      enhance HLA class I expression, rendering liver cells vulnerable to CD8 T-cell 
      attack; and induce HLA class II expression on hepatocytes; or they can 
      differentiate into T(H)2 cells, which produce IL-4, IL-10 and IL-13, cytokines 
      favouring autoantibody production by B lymphocytes. Autoantigen recognition is 
      tightly controlled by regulatory mechanisms, such as those exerted by 
      CD4+CD25(high) regulatory T cells. Numerical and functional regulatory T cell 
      impairment characterises AIH and permits the perpetuation of effector immune 
      responses with ensuing persistent liver destruction. Advances in the study of 
      autoreactive T cells stem mostly from AIH type 2, where the main autoantigen, 
      cytochrome P450IID6 (CYP2D6), is known to enable characterisation of 
      antigen-specific immune responses.
CI  - Copyright 2010 S. Karger AG, Basel.
FAU - Longhi, Maria Serena
AU  - Longhi MS
AD  - Institute of Liver Studies, King's College London School of Medicine at King's 
      College Hospital, London, UK.
FAU - Ma, Yun
AU  - Ma Y
FAU - Mieli-Vergani, Giorgina
AU  - Mieli-Vergani G
FAU - Vergani, Diego
AU  - Vergani D
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20100507
PL  - Switzerland
TA  - Dig Dis
JT  - Digestive diseases (Basel, Switzerland)
JID - 8701186
RN  - 0 (Autoantibodies)
SB  - IM
MH  - *Adaptive Immunity
MH  - Autoantibodies/immunology
MH  - Autoimmunity
MH  - CD4-Positive T-Lymphocytes/immunology
MH  - CD8-Positive T-Lymphocytes/immunology
MH  - Genetic Predisposition to Disease
MH  - Hepatitis, Autoimmune/genetics/*immunology/pathology
MH  - Humans
MH  - Liver/*immunology/pathology
MH  - Lymphocytes/immunology
MH  - Molecular Mimicry
MH  - T-Lymphocytes, Regulatory/immunology
RF  - 47
EDAT- 2010/05/13 06:00
MHDA- 2010/09/11 06:00
CRDT- 2010/05/13 06:00
PHST- 2010/05/13 06:00 [entrez]
PHST- 2010/05/13 06:00 [pubmed]
PHST- 2010/09/11 06:00 [medline]
AID - 000282066 [pii]
AID - 10.1159/000282066 [doi]
PST - ppublish
SO  - Dig Dis. 2010;28(1):63-9. doi: 10.1159/000282066. Epub 2010 May 7.