In vitro study of IgG production and concanavalin A induced suppressor cell function in acute and chronic hepatitis B virus infection

Clin Exp Immunol. 1986 Apr;64(1):50-8.

Abstract

To investigate the relationship between liver damage and immune regulation in hepatitis B virus (HBV) infection, 68 patients with HBsAg in serum and a spectrum of liver damage have been studied and compared with 25 controls. In HBsAg carriers, spontaneous IgG production was elevated only in those with chronic active hepatitis (P less than 0.05) whilst those with less severe inflammation had values comparable to normals. Concanavalin A (Con A) induced suppressor cell regulation of IgG producing cells was impaired in those with chronic active hepatitis (P less than 0.01) and those with chronic persistent hepatitis (P = 0.05) and there was a correlation in both groups of patients with the severity of portal tract inflammation (P less than 0.05). In contrast those with minimal liver damage had values in the normal range. Patients presenting with acute hepatitis B also had elevated spontaneous IgG production (P less than 0.01) and impaired Con A induced suppressor cell regulation of IgG production (P less than 0.01). Sequential study of three patients prior to the detection of HBsAg in serum and subsequently during and after acute hepatitis B showed that such abnormalities were transient and closely related to the onset of liver damage.

MeSH terms

  • Adult
  • Antibody-Producing Cells / drug effects
  • Concanavalin A / pharmacology
  • Female
  • Hepatitis B / immunology*
  • Hepatitis B / pathology
  • Hepatitis B Antigens / analysis
  • Hepatitis delta Antigens
  • Hepatitis, Chronic / immunology*
  • Humans
  • Immunoglobulin G / biosynthesis*
  • In Vitro Techniques
  • Liver / pathology
  • Lymphocyte Activation
  • Male
  • Middle Aged
  • T-Lymphocytes, Regulatory / drug effects
  • T-Lymphocytes, Regulatory / immunology*
  • Time Factors
  • Transaminases / blood

Substances

  • Hepatitis B Antigens
  • Hepatitis delta Antigens
  • Immunoglobulin G
  • Concanavalin A
  • Transaminases