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Characteristics of peripheral blood CD4+CD25+ regulatory T cells and related cytokines in severe atopic dermatitis
Authors:Yun-Ying?Zhang,Ao-Xue?Wang,Lu?Xu,Nan?Shen,Jie?Zhu,Cai-Xia?Tu  author-information"  >  author-information__contact u-icon-before"  >  mailto:tucx@sina.com"   title="  tucx@sina.com"   itemprop="  email"   data-track="  click"   data-track-action="  Email author"   data-track-label="  "  >Email author
Affiliation:1.Department of Dermatology,the 2nd Affiliated Hospital of Dalian Medical University,Liaoning Province,P. R. China;2.Department of Clinical Laboratory,the 2nd Affiliated Hospital of Dalian Medical University,Liaoning Province,P. R. China
Abstract:

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+CD25high 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 ofTeffs were assessed in the absence or presence of autologous Tregs and the TGF-β1 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-β 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.
Keywords:
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