PMID: 2491614Jan 1, 1989Paper

Progression of autoimmune damage in primary biliary cirrhosis: an immunohistochemical study

Autoimmunity
A FloreaniO F James

Abstract

Aberrant MHC Class II antigen expression and the nature of the infiltrating lymphoid cells were studied by immunohistochemical techniques in liver biopsies from 37 patients with Primary biliary cirrhosis (PBC) (11 histological stage I, 13 stage II-III, 13 stage IV) and 15 patients with chronic non autoimmune liver disease. Bile duct epithelial cells expressed HLA-DR, DP and DQ antigens in biopsies from patients with early (Stage I) PBC and less frequently in the late cirrhotic phases of the disease (Stage IV); these observations support the hypothesis that induction of Class II antigens on epithelial cells may be involved in initiating autoimmune responses towards bile duct components. The presence of cytotoxic/suppressor T cells around the bile ducts in Stage I suggests a role for cell mediated destruction of the ducts at this early stage. The nature of the chronic inflammatory cell infiltrate in the portal tracts, periportal areas and lobular parenchyma does not establish the mechanism(s) involved in disease progression. However, the lack of Class II antigen expression on hepatocytes is compatible with the hypothesis that hepatocellular damage is non-specific and may be secondary to the initial bile duct injury.

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Citations

Oct 3, 2003·Veterinary Immunology and Immunopathology·M SpeetiE Westermarck
Sep 26, 2002·Hepatology : Official Journal of the American Association for the Study of Liver Diseases·Hiroto KitaM Eric Gershwin
Aug 1, 1989·Hepatology : Official Journal of the American Association for the Study of Liver Diseases·O F JamesM F Bassendine
Apr 1, 1995·Hepatology : Official Journal of the American Association for the Study of Liver Diseases·D E JonesA G Diamond
Nov 2, 2001·FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology·S C AffordD H Adams
Jan 1, 1990·Annals of the New York Academy of Sciences·R Datema

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