Simultaneous expression of Th1 cytokines and IL-4 confers severe characteristics to type I autoimmune hepatitis in children

Hum Immunol. 2004 Jul;65(7):683-91. doi: 10.1016/j.humimm.2004.03.004.

Abstract

To investigate the immunopathogenic mechanisms of type I autoimmune hepatitis in children, we analyzed by quantitative or semiquantitative reverse transcription-polymerase chain reaction the expression of cytokines interferon (IFN)-gamma, interleukin (IL)-12p40, IL-18, IL-4, IL-10, and IL-12R beta 2. In addition, liver and peripheral blood was collected to investigate the expression of the natural killer T (NKT) cell marker V alpha 24. The presence of NKT cells in hepatic lesions were also identified by immunohistochemistry. The analysis was performed on liver biopsies from 25 children with type I autoimmune hepatitis. As disease controls, we included six children with hepatitis C virus-related chronic hepatitis and nine control livers. The expression of IFN-gamma and IL-12p40 was not detected in controls but was clearly upregulated in pathologic biopsies. In addition, these samples showed an increased expression of IL-18 (p = 0.0003), IL-4 (p = 0.0055), and IL-12R beta 2 (p = 0.007). Western blot analysis confirmed the expression of IL-12p40 and IL-18. However, for IL-18, we detected only the immature biologically inactive polypeptide. The V alpha 24 transcripts were found increased in the liver (p = 0.0007) where V alpha 24(+) cells were also localized, but decreased in peripheral blood mononuclear cells (p = 0.041). In addition to a type I immune response, NKT cells might play a substantial role in the pathogenesis of type I autoimmune hepatitis in children.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adolescent
  • Autoantibodies / blood
  • Biopsy, Needle
  • Blood Chemical Analysis
  • Blotting, Western
  • Child
  • Cytokines / genetics*
  • Cytokines / immunology
  • Cytokines / metabolism
  • Female
  • Gene Expression*
  • Hepatitis, Autoimmune / genetics
  • Hepatitis, Autoimmune / immunology
  • Hepatitis, Autoimmune / pathology*
  • Humans
  • Immunohistochemistry
  • Interferon-gamma / genetics
  • Interleukin-10 / genetics
  • Interleukin-10 / metabolism
  • Interleukin-12 / genetics
  • Interleukin-12 / metabolism
  • Interleukin-12 Subunit p40
  • Interleukin-18 / genetics
  • Interleukin-18 / metabolism
  • Interleukin-4 / genetics*
  • Interleukin-4 / immunology
  • Interleukin-4 / metabolism
  • Killer Cells, Natural / immunology
  • Killer Cells, Natural / metabolism
  • Killer Cells, Natural / pathology
  • Leukocytes, Mononuclear / chemistry
  • Liver / immunology
  • Liver / metabolism
  • Liver / pathology
  • Male
  • Protein Subunits / genetics
  • Protein Subunits / metabolism
  • Receptors, Antigen, T-Cell, alpha-beta / analysis
  • Receptors, Antigen, T-Cell, alpha-beta / genetics
  • Receptors, Interleukin / genetics
  • Receptors, Interleukin / metabolism
  • Receptors, Interleukin-12
  • T-Lymphocytes, Helper-Inducer / immunology
  • T-Lymphocytes, Helper-Inducer / metabolism
  • Th1 Cells / immunology*
  • Th1 Cells / metabolism

Substances

  • Autoantibodies
  • Cytokines
  • Interleukin-12 Subunit p40
  • Interleukin-18
  • Protein Subunits
  • Receptors, Antigen, T-Cell, alpha-beta
  • Receptors, Interleukin
  • Receptors, Interleukin-12
  • Interleukin-10
  • Interleukin-12
  • Interleukin-4
  • Interferon-gamma