Predominant T helper 1 cells in patients with idiopathic portal hypertension

被引:14
作者
Tokushige, K
Yamauchi, K
Komatsu, T
Takasaki, K
Hayashi, N
机构
[1] Tokyo Womens Med Univ, Tokyo Womens Med Coll, Inst Gastroenterol, Div Med,Shinjuku Ku, Tokyo 1628666, Japan
[2] Yokohama Natl Univ, Clin Res Inst, Kanagawa, Japan
关键词
idiopathic portal hypertension; T helper cells 1 and 2 CD4+ T cells; tumor necrosis factor;
D O I
10.1046/j.1440-1746.2000.02330.x
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
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 pf 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. (C) 2000 Blackwell Science Asia Pty Ltd.
引用
收藏
页码:1312 / 1317
页数:6
相关论文
共 25 条
  • [11] MIKKELSEN WILLIAM P., 1965, ANN SURG, V162, P602
  • [12] EXPRESSION OF A TUMOR-NECROSIS-FACTOR-ALPHA TRANSGENE IN MURINE LUNG CAUSES LYMPHOCYTIC AND FIBROSING ALVEOLITIS - A MOUSE MODEL OF PROGRESSIVE PULMONARY FIBROSIS
    MIYAZAKI, Y
    ARAKI, K
    VESIN, C
    GARCIA, I
    KAPANCI, Y
    WHITSETT, JA
    PIGUET, PF
    VASSALLI, P
    [J]. JOURNAL OF CLINICAL INVESTIGATION, 1995, 96 (01) : 250 - 259
  • [13] MOSMANN TR, 1989, ANNU REV IMMUNOL, V7, P145, DOI 10.1146/annurev.iy.07.040189.001045
  • [14] Mwatha JK, 1998, J IMMUNOL, V160, P1992
  • [15] Characteristic changes of peripheral lymphocyte subset in cirrhotic patients with hepatitis C virus - correlation with cirrhosis severity
    Nakano, I
    Fukuda, Y
    Katano, Y
    Kohsaka, T
    Miyazaki, T
    Hayakawa, T
    [J]. HEPATOLOGY RESEARCH, 1999, 15 (01) : 43 - 51
  • [16] OKUDA K, 1984, GASTROENTEROLOGY, V86, P600
  • [17] OKUDA K, 1982, Liver, V2, P176
  • [18] LYMPHOCYTE-RESPONSES AND CYTOKINES
    PAUL, WE
    SEDER, RA
    [J]. CELL, 1994, 76 (02) : 241 - 251
  • [19] Predominant T-Helper 1 cytokine profile of hepatitis B virus nucleocapsid-specific T cells in acute self-limited hepatitis B
    Penna, A
    DelPrete, G
    Cavalli, A
    Bertoletti, A
    DElios, MM
    Sorrentino, R
    DAmato, M
    Boni, C
    Pilli, M
    Fiaccadori, F
    Ferrari, C
    [J]. HEPATOLOGY, 1997, 25 (04) : 1022 - 1027
  • [20] REQUIREMENT OF TUMOR-NECROSIS-FACTOR FOR DEVELOPMENT OF SILICA-INDUCED PULMONARY FIBROSIS
    PIGUET, PF
    COLLART, MA
    GRAU, GE
    SAPPINO, AP
    VASSALLI, P
    [J]. NATURE, 1990, 344 (6263) : 245 - 247