Cellular cytotoxicity against autologous hepatocytes in children with different forms of chronic hepatitis B

Cell-mediated immune reactions play the most important role in the pathogenesis of chronic viral and auto-immune hepatitis. Cellular cytotoxicity (CC) of peripheral blood lymphocytes against autologous hepatocytes isolated from liver biopsies was studied in 29 children with different types of hepati...

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Bibliographic Details
Published in:European journal of pediatrics 1990-09, Vol.149 (12), p.829-832
Main Authors: Keller, K M, Poralla, T, Dienes, H P, Wirth, S, Baumann, W
Format: Article
Language:English
Subjects:
Adolescent
Child
Child, Preschool
Cytotoxicity Tests, Immunologic
Cytotoxicity, Immunologic
DNA, Viral - isolation & purification
Female
Hepatitis B - immunology
Hepatitis B Core Antigens - isolation & purification
Hepatitis B e Antigens - isolation & purification
Hepatitis, Chronic - immunology
Humans
Infant
Liver - cytology
Liver - immunology
Male
Transaminases - blood
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Summary:Cell-mediated immune reactions play the most important role in the pathogenesis of chronic viral and auto-immune hepatitis. Cellular cytotoxicity (CC) of peripheral blood lymphocytes against autologous hepatocytes isolated from liver biopsies was studied in 29 children with different types of hepatitis B surface antigen (HBsAg)-positive hepatitis. Children with chronic hepatitis B showed higher cytotoxicity than control patients. However, a correlation of cytotoxicity to serum amino-transferases, HBeAg-/Anti-HBe-status, and hepatitis B virus DNA in serum could not be found. Children with a higher percentage of hepatitis B core antigen (HBcAg) expression in their liver tissue presented lower CC values, and vice versa. This supports the hypothesis that virus elimination occurs via T-cell attack against HBcAg expressing hepatocytes. Furthermore, children with a longer duration of chronic hepatitis B had considerably higher cytotoxicity values. Possibly, CC plays a role in perpetuating liver damage after infection with hepatitis B virus.
ISSN:0340-6199
1432-1076
DOI:10.1007/BF02072068