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银屑病关节炎患者受刺激的T细胞上CD154(CD40L)表达增加。

Increased expression of CD154 (CD40L) on stimulated T-cells from patients with psoriatic arthritis.

作者信息

Daoussis D, Antonopoulos I, Andonopoulos A P, Liossis S-N C

机构信息

Division of Rheumatology, Department of Internal Medicine, Patras University Hospital, 26504 Rion, Patras Greece.

出版信息

Rheumatology (Oxford). 2007 Feb;46(2):227-31. doi: 10.1093/rheumatology/kel229. Epub 2006 Jul 22.

Abstract

OBJECTIVES

CD40L is a costimulatory molecule and an early activation marker of T-lymphocytes. Based on the hypothesis that activated T-cells may play a role in the pathogenesis of psoriatic arthritis (PsA), we evaluated the level of CD40L expression on T-cells from patients with PsA.

METHODS

We analysed 12 patients with PsA, six patients with rheumatoid arthritis (RA) and four healthy volunteers. T-cell surface expression of CD40L was evaluated using two-colour flow cytometry in (i) the resting state and (ii) following stimulation with phorbol myristate acetate/ionomycin, with or without ciclosporin (CsA)-mediated inhibition.

RESULTS

Expression of CD40L was significantly increased on activated T-cells from patients with PsA, particularly those with active disease, when compared with normal individuals and patients with RA (mean percentages of CD3+ CD40L+ cells: 23.74, 11.59 and 9.57% for patients with active PsA, patients with RA and healthy volunteers, respectively). CsA-mediated inhibition of CD40L induction was equally effective in all study groups.

CONCLUSION

CD40L is overexpressed on T-cells from patients with active PsA. This may indicate a role for CD40L in PsA pathogenesis. Larger-scale studies are warranted to address these issues.

摘要

目的

CD40L是一种共刺激分子,也是T淋巴细胞的早期活化标志物。基于活化的T细胞可能在银屑病关节炎(PsA)发病机制中起作用的假说,我们评估了PsA患者T细胞上CD40L的表达水平。

方法

我们分析了12例PsA患者、6例类风湿关节炎(RA)患者和4名健康志愿者。使用双色流式细胞术评估(i)静息状态下和(ii)用佛波酯/离子霉素刺激后,有无环孢素(CsA)介导的抑制作用时T细胞表面CD40L的表达。

结果

与正常个体和RA患者相比,PsA患者活化T细胞上CD40L的表达显著增加,尤其是那些患有活动性疾病的患者(活化的PsA患者、RA患者和健康志愿者中CD3+CD40L+细胞的平均百分比分别为23.74%、11.59%和9.57%)。CsA介导的对CD40L诱导的抑制在所有研究组中同样有效。

结论

活动性PsA患者的T细胞上CD40L过度表达。这可能表明CD40L在PsA发病机制中起作用。有必要进行更大规模的研究来解决这些问题。

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