title: Cytokine production by peripheral blood mononuclear cells in IgA nephropathy.
abstract: The regulation of cytokine production and T cell proliferation by other cytokines is mandatory in mediating inflammatory responses but the full understanding is far from complete. We have previously reported increased production of IL-2 and IL-2 receptors (IL-2R) in IgA nephropathy. The present study was undertaken to examine other cytokine production during T cell activation in IgA nephropathy. Peripheral blood mononuclear cells (PBMC) from 17 IgA nephritic patients and 14 controls were cultured with phytohaemagglutinin and phorbol myristate acetate for 48 h for maximal cytokine production. IL-2Rs and IL-4 receptors (IL-4Rs) expressed on cultured PBMC were studied by a radioimmunoassay using monoclonal antibodies against these receptors. Although the total cellular IL-2R expression and percentages of T helper and T suppressor cells did not differ between the patients and controls, there was a significant increase in activated T helper cells expressing IL-2R in patients with IgA nephropathy. The total cellular IL-4R expression was elevated in IgA nephritic patients (P less than 0.005). IL-2 production by PBMC was raised in IgA nephritic patients compared with controls (P less than 0.05) but no difference in IL-4 or IL-6 production was observed. The interferon-gamma production by PBMC was significantly increased in patients with IgA nephropathy (P less than 0.025). No correlation was observed between individual cytokine levels. Our data suggest there are selective increases in cytokine production in IgA nephropathy.
authors.affiliation: Department of Medicine, Chinese University of Hong Kong, Prince of Wales Hospital.
authors.forename: K N
authors.initials: KN
authors.lastname: Lai
authors.forename: J C
authors.initials: JC
authors.lastname: Leung
authors.forename: P K
authors.initials: PK
authors.lastname: Li
authors.forename: S F
authors.initials: SF
authors.lastname: Lui
mesh_terms: D016207:Cytokines / Q000096:biosynthesis*; D005922:Glomerulonephritis, IGA / Q000276:immunology*; D006801:Humans; D007371:Interferon-gamma / Q000096:biosynthesis; D007376:Interleukin-2 / Q000096:biosynthesis; D007963:Leukocytes, Mononuclear / Q000276:immunology / Q000378:metabolism*; D008213:Lymphocyte Activation; D015375:Receptors, Interleukin-2 / Q000096:biosynthesis; D019948:Receptors, Interleukin-4; D011975:Receptors, Mitogen / Q000096:biosynthesis
chemical_list: D016207:Cytokines; D007376:Interleukin-2; D015375:Receptors, Interleukin-2; D019948:Receptors, Interleukin-4; D011975:Receptors, Mitogen; D007371:Interferon-gamma