Volume 59, Issue 5 pp. 643-646
Brief Report

Regulatory T cells and CTLA-4 in idiopathic nephrotic syndrome

Shoji Tsuji

Shoji Tsuji

Department of Pediatrics, Kansai Medical University, Osaka, Japan

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Takahisa Kimata

Takahisa Kimata

Department of Pediatrics, Kansai Medical University, Osaka, Japan

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Sohsaku Yamanouchi

Sohsaku Yamanouchi

Department of Pediatrics, Kansai Medical University, Osaka, Japan

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Tetsuya Kitao

Tetsuya Kitao

Department of Pediatrics, Kansai Medical University, Osaka, Japan

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Jiro Kino

Jiro Kino

Department of Pediatrics, Kansai Medical University, Osaka, Japan

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Chikushi Suruda

Chikushi Suruda

Department of Pediatrics, Kansai Medical University, Osaka, Japan

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Kazunari Kaneko

Corresponding Author

Kazunari Kaneko

Department of Pediatrics, Kansai Medical University, Osaka, Japan

Correspondence: Kazunari Kaneko, MD, PhD, Department of Pediatrics, Kansai Medical University, 2-5-1 Shin-machi, Hirakata-shi, Osaka 573 1010, Japan. Email: [email protected]Search for more papers by this author
First published: 23 May 2017
Citations: 33

Abstract

The pathogenesis of idiopathic nephrotic syndrome (INS) remains unknown. Recently, it was postulated that suppression of regulatory T cells (Treg) leads to massive proteinuria in INS, although there is some controversy. Considering the important role of cytotoxic T-lymphocyte-associated protein 4 (CTLA-4) in Treg-mediated immune suppression, the aim of this study was therefore to clarify the involvement of Treg and CTLA-4 in the pathogenesis of INS. Fifteen patients with INS were enrolled. Their blood was sampled twice, once at onset and once at remission induced by glucocorticoid. Although median Treg number was significantly lower at onset than in healthy children, it increased at remission. Similarly, serum CTLA-4 concentration significantly increased at remission compared with onset. Furthermore, a positive significant correlation was observed between Treg number and serum CTLA-4 level. This suggests that Treg and CTLA-4 are involved in the induction of remission in INS.

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