Peripheral CD8+/CD25+ lymphocytes may be implicated in hepatocellular injuries in patients with acute-onset autoimmune hepatitis

J Gastroenterol. 2004 Jul;39(7):649-53. doi: 10.1007/s00535-003-1360-z.

Abstract

Background: The mechanism of liver injuries in autoimmune hepatitis (AIH) is not fully understood, especially because the onset is insidious and the clinical courses fluctuate with spontaneous exacerbation and improvement even without immunosuppressive therapies.

Methods: Eleven patients with acute-onset AIH, some of whom were without hypergammaglobulinemia or anti-nuclear antibodies, and 41 patients with chronic AIH were compared serologically, biochemically, and histologically to determine differences in liver injuries between patients with acute-onset and chronic AIH. All patients fulfilled the diagnostic criteria according to a scoring system proposed in 1999.

Results: Lymphocytes with CD8+/CD25+ markers in pretreatment blood were significantly more prevalent in acute-onset than chronic AIH patients (24% vs 14%; P < 0.05). After treatment, however, CD8+/CD25+ lymphocytes were fewer in patients with acute-onset than in those with chronic AIH at 1 and 2 weeks ( P = 0.0001). No other differences were noted in clinical characteristics or immunological parameters between patients with acute-onset and those with chronic AIH. In a patient with typical acute-onset AIH, CD8+/CD25+ lymphocytes increased and decreased in parallel with the activity of liver disease.

Conclusions: Activated CD8+ T lymphocytes with CD25 markers may be implicated in the development of acute-onset AIH.

Publication types

  • Case Reports

MeSH terms

  • Acute Disease
  • Adult
  • Autoantibodies / blood
  • CD8-Positive T-Lymphocytes / immunology*
  • Chronic Disease
  • Female
  • Hepatitis, Autoimmune / immunology*
  • Hepatitis, Autoimmune / metabolism
  • Hepatitis, Autoimmune / pathology
  • Humans
  • Liver / metabolism
  • Liver / pathology*
  • Lymphocyte Subsets
  • Lymphocytes / immunology*
  • Receptors, Interleukin-2 / analysis*

Substances

  • Autoantibodies
  • Receptors, Interleukin-2