Open AccessLymphocyte subsets and β 2 ‐microglobulin expression in chronic hepatitis C/non‐A, non‐B. Effects of interferon‐alpha treatment
Author(s) -
WEJSTÅL R.,
NORKRANS G.,
WEILAND O.,
SCHVARCZ R.,
FUCHS D.,
WACHTER H.,
FRYDEN A.,
GLAUMANN H.
Publication year - 1992
Publication title -
clinical & experimental immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.329
H-Index - 135
eISSN - 1365-2249
pISSN - 0009-9104
DOI - 10.1111/j.1365-2249.1992.tb02999.x
Subject(s) - beta 2 microglobulin , cd8 , cytotoxic t cell , immunology , hepatocyte , liver biopsy , medicine , alpha interferon , interferon , biopsy , antigen , biology , in vitro , biochemistry
SUMMARY Thirty‐three patients with chronic hepatitis C/non‐A. non‐B were included in a randomized controlled study of interferon‐alpha 2b (IFN‐α2b) treatment, 3 × 10 6 U three times weekly for 36 weeks. Using an immunoperoxidase technique, frozen liver biopsy specimens were examined with MoAbs for the presence of T helper cells (CD4), T suppressor/cytotoxic cells (CD8), total T cells (CD2) and B cells (CD22) before and after treatment, β 2 ‐microglohulin (β 2 ‐MG) expression on hepatocytes was scmiquantified using a scoring system on sections from paraffin‐embedded biopsy specimens. Serum levels of β 2 ‐MG were analysed with a radioimmunoassay technique. Intralobular T helper and T suppressor/cytotoxic cells declined significantly in the treated patients but not in the controls. The portal CD4/CD8 ratio did not change. Before treatment, serum β 2 ‐MG levels and hepatocyte β 2 ‐MG expression were significantly higher in patients with chronic active hepatitis compared to patients with chronic persistent hepatitis. Serum β 2 ‐MG levels increased significantly in responders during IFN treatment, with a maximum after 12 weeks. However, in the liver, the hepatocyte β 2 ‐MG expression was significantly decreased after treatment. Thus. IFN‐α treatment docs not seem to induce an increased HLA class I antigen hepatocyte expression in chronic non‐A, non‐B hepatitis, which favours the hypothesis that its anti‐viral effects are more important in modulating the disease activity.