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Nephrol Dial Transplant (2001) 16: 1783-1789
© 2001 European Renal Association-European Dialysis and Transplant Association

Th2 predominance at the single-cell level in patients with IgA nephropathy

Itaru Ebihara, Kouichi Hirayama, Satoshi Yamamoto, Kaori Muro, Kunihiro Yamagata and Akio Koyama

Department of Internal Medicine, Institute of Clinical Medicine, University of Tsukuba, Ibaraki, Japan

Background. Abnormalities of lymphocyte function have been reported to be involved in the pathogenesis of IgA nephropathy (IgA-N). The aim of this study was to investigate helper T (Th) predominance at the single-cell level, one of the abnormalities of lymphocyte function in IgA-N.

Methods. Using flowcytometry, we assessed the levels of circulating Th cells in IgA-N patients (n=30), and in normal individuals (n=30) based on the expression of intracellular Th1 cytokines for interleukin-2 (IL-2) and interferon-{gamma} (IFN-{gamma}), and of intracellular Th2 cytokines for IL-4, IL-10, and IL-13. Because the production of each cytokine had a specific time course, we examined cytokine synthesis at 3, 6, 9, and 12 h after stimulation.

Results. The percentages of IL-2-positive Th cells from IgA-N patients were significantly lower than in normal individuals at 6, 9, and 12 h, with the difference becoming greater with time. The number of IFN-{gamma}-positive Th cells in IgA-N patients was significantly lower than in normal individuals at 9 h, and the number of IFN-{gamma}-positive Th cells increased more at 12 h than at 3 h in both groups. IL-4 and IL-13 expression was increased in patients with IgA-N at 6 h compared with normal individuals. In IgA-N patients, the percentage of IL-10-positive Th cells was significantly higher than that in normal individuals at each time-point.

Conclusion. A polarization toward Th2 response at the stimulated lymphocyte level may lead to immune abnormalities in IgA-N.

Keywords: IgA nephropathy; helper T cell; cytokine; single-cell level; time course

Correspondence and offprint requests to: Kouichi Hirayama, MD, PhD, Department of Internal Medicine, Institute of Clinical Medicine, University of Tsukuba, 1-1-1 Ten-nodai, Tsukuba, Ibaraki 305-8575, Japan.


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