ArticleClinical and experimental immunology1994
Profiles of immunoregulatory cytokine production in vitro in patients with IgA nephropathy and their kindred.
Article in Clinical and experimental immunology, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- B cell-derived IL-4 acts on podocytes to induce proteinuria and foot process effacement.JCI insight · 2017Article
- Pathogenesis of immunoglobulin A nephropathy: recent insight from genetic studies.Annual review of medicine · 2013Review
- Down-regulation of core 1 beta1,3-galactosyltransferase and Cosmc by Th2 cytokine alters O-glycosylation of IgA1.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2010Article
- T cell cytokine polarity as a determinant of immunoglobulin A (IgA) glycosylation and the severity of experimental IgA nephropathy.Clinical and experimental immunology · 2008Article
- For further investigations in IgA nephropathy the approach from phenotype to genotype is welcome.Clinical and experimental immunology · 2002Article
- T cell cytokines determine the severity of experimental IgA nephropathy by regulating IgA glycosylation.Clinical and experimental immunology · 2001Article
- Increased IL-10 production by stimulated whole blood cultures in primary IgA nephropathy.Clinical and experimental immunology · 1998Article
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Authors and funding
7 authors.
Funding
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Abstract
We hypothesized that the altered immunoglobulin synthesis and/or lymphocyte function apparent in patients with IgA nephropathy (IgAN) is due to a primary defect in lymphokine regulation. In addition, we reasoned that such changes in lymphokine production might be, at least partially, genetically determined. To assess the extent of lymphocyte abnormalities, we investigated the profile of cytokine production from peripheral blood mononuclear cells (PBMC) in 34 IgAN patients and 44 of their first degree relatives, 10 of whom had persistent microhaematuria. Compared with healthy volunteers (n = 34), PBMC from patients showed increased IL-2 production both spontaneously or after phytohaemagglutinin (PHA) (20 micrograms/ml) stimulation, whereas IL-4 and interferon-gamma (IFN-gamma) production were significantly higher only after stimulation. Microhaematuric relatives had a similar pattern of cytokine production, whereas non-microhaematuric relatives showed no significant difference versus normals. The altered pattern of cytokine production appeared to be quite specific to IgAN patients and their microhaematuric relatives, because patients with other forms of primary glomerulonephritis (n = 17) did not differ from normal individuals. Patients and relatives that hyperproduced IL-4 were also hyperproducers of IL-2. No such congruence was seen in any other group or with any other pairing of cytokines. We propose that a subpopulation of IgAN patients bear lymphocytes intrinsically hyperresponsive. Among those individuals such hyperresponsiveness may be causally related to the pathogenesis and/or character of IgAN.
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