CD4 CD25high regulatory T cells are not impaired in patients with primary Sjogren's syndrome
CD4 CD25high regulatory T cells are not impaired in patients with primary Sjogren's syndrome
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DOI：
10.1016/j.jaut.2005.01.015
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发表时间：
2005-05-01
影响因子：
12.8
通讯作者：
Mariette, X
中科院分区：
文献类型：
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作者：
Gottenberg, JE;Lavie, F;Mariette, X
在自身免疫动物模型中，C134 CD25(高) T 细胞在控制自身免疫过程中发挥着关键作用。很少有研究调查这些细胞在人类自身免疫性疾病中的作用。我们的目的是调查原发性干燥综合征 (pSS) 患者外周血中的 C134 CD25(高) T 细胞。采用流式细胞术测定了 21 名按美国-欧洲共识组标准确定的 pSS 患者和两组对照（18 名机械性腰背痛患者和 15 名健康献血者）的血液 C134 CD25（高）T 细胞比例。使用共培养测定评估 C134 CD25 细胞的抑制功能。通过流式细胞术检查 C134 CD25 T 细胞的 Vbeta 库。 C134 CD25 T 细胞的比例取决于患者和对照组的年龄。在年龄匹配比较中，pSS 患者和对照组之间总 C134 CD25（低）T 细胞的比例没有观察到显着差异（P = 0.36）。相比之下，pSS 患者的 C134 CD25 高水平显着增加（对照组为 8.5% vs 4.1%，P = 0.04）。在疾病较活跃的患者中，C134 CD25 高细胞比例略有增加，但并不显着。 pSS患者中的C134 CD25 T细胞有效抑制CD4 CD25(-)自体应答T细胞的增殖。 pSS 患者的调节性 T 细胞的 Vbeta 库是多克隆的，与对照组相比没有显着限制。尽管存在持续的自身免疫，但通过反应性反馈，已确诊 pSS 的患者中功能性 C134 CD25 高调节细胞有所增加。这些结果表明，pSS 的发生并不是由于 C134 CD25 高调节性 T 细胞水平降低，也不是响应细胞增殖抑制缺陷所致。 (c) 2005 Elsevier Ltd. 保留所有权利。
In animal models of autoinimunity, C134 CD25(high) T cells play a key role in the control of the autoimmune process. Few studies have investigated the role of these cells in human autoinumme diseases. We aimed to investigate C134 CD25(high) T cells in the peripheral blood of patients with primary Sjbgren's syndrome (pSS). The proportion of blood C134 CD25(high) T cells was determined by flow cytometry in 21 patients with pSS as determined by the American-European consensus group criteria and two groups of controls (18 patients with lumbar back pain of mechanical origin and 15 healthy blood donors). The suppressive function of C134 CD25 cells was assessed using co-culture assays. The Vbeta repertoire of C134 CD25 T cells was examined by flow cytometry. The proportion of C134 CD25 T cells depended on age in patients and controls. In an age-matched comparison, no significant difference was observed in the proportion of total C134 CD25(low) T cells between patients with pSS and controls (P = 0.36). In contrast, the pool of C134 CD25 high was significantly increased in patients with pSS (8.5% vs 4.1 % in controls, P = 0.04). There was a slight but not significant higher proportion of C134 CD25 high Cells in patients with a more active disease. C134 CD25 T cells in patients with pSS effectively suppressed the proliferation of CD4 CD25(-) autologous responder T cells. The Vbeta repertoire of regulatory T cells from patients with pSS was polyclonal and was not significantly restricted as compared with that in controls. Functional C134 CD25 high regulatory cells are increased in patients with established pSS, through a reactive feedback, despite ongoing autoimmunity. These results suggest that pSS does not occur as a result of reduced level of C134 CD25 high regulatory T cells, nor as a defect of inhibition of proliferation of responder cells. (c) 2005 Elsevier Ltd. All rights reserved.