慢性湿疹患者外周血CD4^+CD25^+Foxp3^+调节性T细胞的检测

Detection of CD4^+CD25^+Foxp3^+ regulatory T cells in peripheral blood of patients with chronic eczema

目的研究外周血CD4+CD25+Foxp3+调节性T细胞(Treg细胞)数量改变所致的细胞免疫抑制效应在慢性湿疹发病机制中的作用。方法采用免疫荧光标染技术,经流式细胞仪检测30例慢性湿疹患者和33例正常人外周血CD4+CD25+T细胞数量及胞内转录因子Foxp3(forkhead box p3)表达水平。结果慢性湿疹患者外周血CD4+CD25+Foxp3+Treg细胞数量比正常人对照组明显下降(P<0.001)。结论慢性湿疹患者外周血CD4+CD25+Foxp3+调节性T细胞数量下降导致参与IV型变态反应的效应性T细胞功能活性增强,这可能是湿疹发病机制之一。

Objective To investigate the suppressive effects of peripheral CD4^＋ CD25^＋ Foxp3^＋ regulatory T cells （Tregs） on cell immunity in the pathogenesis of chronic eczema. Methods The expression of transcription factor Foxp3 and inhibitory membrane molecules, e.g. cytotoxic T lypmphacyte associated antigen - 4 （ CTLA - 4 ）, glucocorticoid - induced TNF receptor family - related gene（GITR） and programmed death - 1 （ PD - 1 ） were determined by three - color flow cytometry in peripheral CD4^ ＋ CD25^ ＋ Foxp3^ ＋ regulatory T cells in peripheral bloood of 30 patients with chronic eczema and 33 normal controls. Highly purified CD4^ ＋ CD25 ^＋ T cells were obtained from peripheral blood by using immunomagnetic beads, and the production of intracellular suppressor cytokines such as interleukin- 10（IL- 10） and transforming growth factor - β （TGF - β） was determined by cytometry. Results The quantity of CD4^＋ CD25^＋ Foxp3^＋ Tregs was decreased significantly in peripheral blood of patients with chronic eczema （5.0% ± 1.0% ） in comparison with that of normal controls（6.4% ± 2.1% ） （ P 〈 0. 001 ）. The expressions of CTLA - 4, GITR and PD - 1 was significantly stronger in patients （2.8 % ± 1.3 %, 12.7 % ± 2.5 % and 1.9 % ± 1.1%, respectively） than that of the controls（ 1.3% ± 1.0% ,9.5% ± 2.4% and 1.3% ± 0.6% ,respectively （P 〈 0.001, P 〈 0.001 and P 〈 0.01 ,respectively）. Conclusion Herpes simplex virus infection may result in the activation and proliferation of CD4^＋ CD25^＋ Tregs, the expression of high levels negative costimulatory molecules on the cell surface and secretion of suppressive cytokines, which may lead to the inhibition of antiviral immune responses via multiple mechanisms.