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Erschienen in: Rheumatology International 4/2012

01.04.2012 | Original Article

Elevated Th17 cells are accompanied by FoxP3+ Treg cells decrease in patients with lupus nephritis

verfasst von: Qian Xing, Bin Wang, Houheng Su, Jiajia Cui, Jinghua Li

Erschienen in: Rheumatology International | Ausgabe 4/2012

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Abstract

To investigate the variations of T-helper 17 (Th17) and regulatory T (Treg) cells in patients with lupus nephritis (LN), a total of 60 systemic lupus erythematosus patients and 28 healthy controls (HCs) were enrolled. The frequency of Th17 cells and Treg cells in peripheral blood mononuclear cells (PBMCs) was evaluated by flow cytometric analysis. The serum concentrations of interleukin-17 (IL-17) and transforming growth factor-beta 1 (TGF-β1) were measured by enzyme-linked immunosorbent assay (ELISA). The results demonstrated in LN patients a significant decrease in the frequency of CD4+CD25high and CD4+CD25+FoxP3+ T cells and a significant increase in the frequency of Th17 cells in peripheral blood, and the ratio of Th17 to Treg cell frequency was significantly increased along with increased SLEDAI scores. LN patients had a lower percentage and expression of FoxP3 in CD4+CD25high T cells than SLE patients without nephritis. The concentration of TGF-β1 was found decreased in SLE patients compared with that from healthy controls, though no significant difference was found between LN patients and SLE patients without nephritis. The expression of IL-17 levels in LN patients exhibited a significant increase compared with patients without nephritis and healthy controls. Based on our results, the significantly elevated Th17 cells are accompanied by FoxP3+ Treg cells decrease in lupus nephritis, suggesting that Th17/Treg functional imbalance may be involved in the pathogenesis of renal damage in SLE patients.
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Metadaten
Titel
Elevated Th17 cells are accompanied by FoxP3+ Treg cells decrease in patients with lupus nephritis
verfasst von
Qian Xing
Bin Wang
Houheng Su
Jiajia Cui
Jinghua Li
Publikationsdatum
01.04.2012
Verlag
Springer-Verlag
Erschienen in
Rheumatology International / Ausgabe 4/2012
Print ISSN: 0172-8172
Elektronische ISSN: 1437-160X
DOI
https://doi.org/10.1007/s00296-010-1771-0

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