Document Detail


The role of natural killer (NK) and NK T cells in the loss of tolerance in murine primary biliary cirrhosis.
MedLine Citation:
PMID:  22519590     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
One of the major obstacles in dissecting the mechanism of pathology in human primary biliary cirrhosis (PBC) has been the absence of animal models. Our laboratory has focused on a model in which mice, following immunization with a xenobiotic chemical mimic of the immunodominant autoepitope of the E2 component of pyruvate dehydrogenase complex (PDC-E2), develop autoimmune cholangitis. In particular, following immunization with 2-octynoic acid (a synthetic chemical mimic of lipoic acid-lysine located within the inner domain of PDC-E2) coupled to bovine serum albumin (BSA), several strains of mice develop typical anti-mitochondrial autoantibodies and portal inflammation. The role of innate immune effector cells, such as natural killer (NK) cells and that NK T cells, was studied in this model based on the hypothesis that early events during immunization play an important role in the breakdown of tolerance. We report herein that, following in-vivo depletion of NK and NK T cells, there is a marked suppression of anti-mitochondrial autoantibodies and cytokine production from autoreactive T cells. However, there was no change in the clinical pathology of portal inflammation compared to controls. These data support the hypothesis that there are probably multiple steps in the natural history of PBC, including a role of NK and NK T cells in initiating the breakdown of tolerance. However, the data suggest that adaptive autoimmune effector mechanisms are required for the progression of clinical disease.
Authors:
S Shimoda; K Tsuneyama; K Kikuchi; K Harada; Y Nakanuma; M Nakamura; H Ishibashi; S Hisamoto; H Niiro; P S C Leung; A A Ansari; M E Gershwin; K Akashi
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Clinical and experimental immunology     Volume:  168     ISSN:  1365-2249     ISO Abbreviation:  Clin. Exp. Immunol.     Publication Date:  2012 Jun 
Date Detail:
Created Date:  2012-04-23     Completed Date:  2012-06-20     Revised Date:  2013-06-05    
Medline Journal Info:
Nlm Unique ID:  0057202     Medline TA:  Clin Exp Immunol     Country:  England    
Other Details:
Languages:  eng     Pagination:  279-84     Citation Subset:  IM    
Copyright Information:
© 2012 The Authors. Clinical and Experimental Immunology © 2012 British Society for Immunology.
Affiliation:
Medicine and Biosystemic Science, Kyushu University Graduate School of Medical Sciences, Fukuoka, Japan.
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MeSH Terms
Descriptor/Qualifier:
Animals
Autoantibodies / blood
Autoantigens / immunology
Biomimetic Materials / chemistry
Cattle
Cells, Cultured
Cytokines / blood
Dihydrolipoyllysine-Residue Acetyltransferase / chemistry,  immunology*,  metabolism
Disease Models, Animal
Humans
Immune Tolerance*
Immunization
Immunodominant Epitopes / chemistry
Killer Cells, Natural / immunology,  metabolism*,  pathology
Liver Cirrhosis, Biliary / immunology*
Lymphocyte Depletion
Mice
Mice, Inbred C57BL
Mitochondria / immunology*,  metabolism
Mitochondrial Proteins / chemistry,  immunology*,  metabolism
Natural Killer T-Cells / immunology,  metabolism*,  pathology
Peptide Fragments / administration & dosage,  chemistry,  metabolism
Serum Albumin, Bovine / administration & dosage,  chemistry
Thioctic Acid / administration & dosage,  chemistry,  metabolism
Grant Support
ID/Acronym/Agency:
DK067003/DK/NIDDK NIH HHS
Chemical
Reg. No./Substance:
0/Autoantibodies; 0/Autoantigens; 0/Cytokines; 0/Immunodominant Epitopes; 0/Mitochondrial Proteins; 0/Peptide Fragments; 0/Serum Albumin, Bovine; 62-46-4/Thioctic Acid; EC 2.3.1.12/Dihydrolipoyllysine-Residue Acetyltransferase; EC 2.3.1.12/Dlat protein, mouse
Comments/Corrections

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