title: Characteristic cytokine products of Th1 and Th2 cells in hemodialysis patients.
abstract: Dysfunction of the host defense against infection in hemodialysis (HD) patients has major clinical and socioeconomic implications. T helper type 1 (Th1) and type 2 (Th2) cytokines are implicated in regulating the immune responses and, therefore, may be involved in impaired status. The present study was designed to examine Th1 and Th2 cytokine profiles in 22 stable HD patients (aged 63 +/- 11 years) and 22 healthy controls (aged 60 +/- 6 years). The T cell activity was significantly retarded in HD patients as compared with normal persons. The proportions of T cytotoxic/suppressor cells and natural killer cells were significantly higher in HD patients than in controls. In contrast, the proportions of T helper/inducer and B cells were significantly lower in HD patients than in controls. The production of interleukin (IL) 2, which is involved in cell-mediated immune responses, and the production of IL-4 and IL-10, which affect humoral immunity, were significantly lower in patients than in controls. The production of IL-12 by macrophages and of interferon gamma by Th1 cells was significantly higher in HD patients than in controls. The concentration of plasma sIL-2R was significantly higher in patients than in controls. These results suggest that both cellular immunity induced by Th1 and humoral immunity induced by Th2 decrease in HD patients, but that improved IL-12 secretion by macrophages activated natural killer cells to produce interferon gamma, which in turn induced macrophage activity.
authors.affiliation: Department of Public Health, Gunma University School of Medicine, Gunma, Japan.
authors.forename: Y
authors.initials: Y
authors.lastname: Daichou
authors.forename: S
authors.initials: S
authors.lastname: Kurashige
authors.forename: S
authors.initials: S
authors.lastname: Hashimoto
authors.forename: S
authors.initials: S
authors.lastname: Suzuki
mesh_terms: D000328:Adult; D000368:Aged; D018941:Antigens, CD19 / Q000032:analysis; D001402:B-Lymphocytes / Q000737:chemistry / Q000166:cytology / Q000187:drug effects; D015496:CD4-Positive T-Lymphocytes / Q000166:cytology / Q000187:drug effects; D016207:Cytokines / Q000096:biosynthesis* / Q000276:immunology; D005260:Female; D006801:Humans; D007371:Interferon-gamma / Q000096:biosynthesis / Q000276:immunology; D016753:Interleukin-10 / Q000096:biosynthesis / Q000276:immunology; D018664:Interleukin-12 / Q000096:biosynthesis / Q000276:immunology; D007376:Interleukin-2 / Q000096:biosynthesis / Q000276:immunology; D015847:Interleukin-4 / Q000096:biosynthesis / Q000276:immunology; D007676:Kidney Failure, Chronic / Q000276:immunology / Q000378:metabolism* / Q000628:therapy; D007958:Leukocyte Count; D008297:Male; D008875:Middle Aged; D010835:Phytohemagglutinins; D006435:Renal Dialysis; D018417:Th1 Cells / Q000276:immunology / Q000378:metabolism*; D018418:Th2 Cells / Q000276:immunology / Q000378:metabolism*
chemical_list: D018941:Antigens, CD19; D016207:Cytokines; D007376:Interleukin-2; D010835:Phytohemagglutinins; D016753:Interleukin-10; D018664:Interleukin-12; D015847:Interleukin-4; D007371:Interferon-gamma