Characteristics of peripheral blood CD4+CD25+regulatory T cells and related cytokines in severe atopic dermatitis

被引:20
作者
Zhang, Yun-Ying [1 ]
Wang, Ao-Xue [1 ]
Xu, Lu [1 ]
Shen, Nan [1 ]
Zhu, Jie [2 ]
Tu, Cai-Xia [1 ]
机构
[1] Dalian Med Univ, Affiliated Hosp 2, Dept Dermatol, 467 Zhongshan Rd, Dalian 116027, Liaoning Provin, Peoples R China
[2] Dalian Med Univ, Affiliated Hosp 2, Dept Clin Lab, 467 Zhongshan Rd, Dalian 116027, Liaoning Provin, Peoples R China
基金
中国国家自然科学基金;
关键词
atopic dermatitis; regulatory T cells; effector T cells; INTERFERON-GAMMA; EXPRESSION; INTERLEUKIN-10; CHILDREN; DISEASE; CD39;
D O I
10.1684/ejd.2015.2709
中图分类号
R75 [皮肤病学与性病学];
学科分类号
100206 ;
摘要
Background: Regulatory T cells (Tregs) have been suggested to play a role in the pathogenesis of atopic dermatitis (AD). However, alterations in the ability of Tregs remain to be determined. Objectives: To investigate the expression of various surface receptors on CD4(+)CD25(high) regulatory T cells and to investigate their capacity for inhibiting the proliferation of CD4(+) CD25(-) effector T cells (Teffs). Materials and methods: Peripheral blood samples were obtained from 15 patients with severe atopic dermatitis (AD) and 20 control subjects. FACs was then carried out to analyze the expression levels of FoxP3, CD152 (CTLA-4), CD39, CD73, CD223 (LAG-3), CCR4, CCR5, and CCR10 on Tregs. The proliferative responses of Teffs were assessed in the absence or presence of autologous Tregs and the TGF-beta 1 and IL-10 levels in the culture supernatant and sera were detected by enzyme-linked immunosorbent assay (ELISA). Results: The CD152, CD39, CD73, CCR4, and CCR5 expression levels on Tregs were higher in patients with severe AD than in the controls. Tregs showed an attenuated suppressive function of the proliferation of autologous Teffs in severe AD. The concentrations of IL-10 and TGF-beta in the culture supernatants of Tregs were lower in the AD group than in the control. Conclusion: The attenuated ability of Tregs to suppress Teff proliferation may be responsible for the autoimmune reaction of severe AD.
引用
收藏
页码:240 / 246
页数:7
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