Predominant T helper 1 cells in patients with idiopathic portal hypertension

J Gastroenterol Hepatol. 2000 Nov;15(11):1312-7.

Abstract

Background: The pathologic mechanism of idiopathic portal hypertension (IPH) is unknown. Because cytokines and the balance of T helper (h) 1 and Th2 CD4+ T cells have been reported to be important for regulating the immune response, in the present study we investigated the role of cytokines and the distribution of cytokine-producing cells in IPH patients.

Methods: Serum levels of tumor necrosis factor (TNF)-alpha, soluble TNF receptor-I, -II, interferon (IFN)-gamma and interleukin (IL)-4 were measured in IPH patients, fatty liver patients, chronic hepatitis patients and control subjects. The percentages of Th0, Th1 and Th2 CD4+ T cells were examined in peripheral and spleen lymphocytes in IPH patients by intracellular staining.

Results: Serum levels of TNF-alpha, soluble TNF receptor-I, interferon-gamma and IL-4 of IPH patients were not increased in comparison with control subjects. Only the mean value of soluble TNF receptor-II was significantly higher than that of control subjects and fatty liver patients. The ratios of Th1 and Th2 in both peripheral and spleen lymphocytes of IPH patients were significantly increased compared with the ratios found in peripheral lymphocytes of control subjects. The increase in the ratios was due to a decrease in the percentage of Th2 CD4+ T cells.

Conclusions: These results suggest that the imbalance of Th1 and Th2 CD4+ T cells and TNF may be associated with the pathogenesis of IPH.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Aged
  • Cytokines / physiology*
  • Etanercept
  • Female
  • Flow Cytometry
  • Humans
  • Hypertension, Portal / etiology
  • Hypertension, Portal / immunology*
  • Immunoglobulin G / immunology
  • Male
  • Middle Aged
  • Receptors, Tumor Necrosis Factor / immunology
  • Th1 Cells / immunology*
  • Th2 Cells / immunology
  • Tumor Necrosis Factor-alpha / immunology

Substances

  • Cytokines
  • Immunoglobulin G
  • Receptors, Tumor Necrosis Factor
  • Tumor Necrosis Factor-alpha
  • Etanercept