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原发性干燥综合征患者外周血T细胞的表型和功能异常。

Phenotypic and functional abnormalities in the peripheral blood T-cells of patients with primary Sjogren's syndrome.

作者信息

Aziz K E, McCluskey P J, Wakefield D

机构信息

Department of Immunopathology, Prince Henry Hospital, NSW Australia.

出版信息

Cytometry. 1994 Mar 15;18(1):35-41. doi: 10.1002/cyto.990180108.

Abstract

Changes in regulatory T-cell subset (including the recently described CD4 helper inducers or suppressor inducers) balance in the peripheral blood may play a role in the pathogenesis of primary Sjogren's syndrome (SS). Direct immunofluorescence and flow cytometry were used to quantitate and analyse peripheral blood lymphocytes in 15 patients with primary SS and 15 control subjects. A reduction in the percentage of circulating CD4 lymphocytes was observed in patients with SS. There was no quantitative abnormality in the percentage of circulating CD4+ 2H4+ (suppressor inducer), CD4+ 4B4+ (helper inducer), CD2, CD3, CD8, CD8+ 2H4+, CD8+ 4B4+, CD25 (IL-2R), CD19, CD16, CD57 lymphocytes in the patients. Circulating CD8 lymphocytes expressing the activation marker HLA-DR were increased in the patients. The functional status of peripheral blood lymphocytes was assessed by PHA (phytohaemagglutinin) stimulation followed by monitoring their proliferative response by radiolabelled thymidine uptake and expression of CD25 (Interleukin-2 receptor). A reduction in the proliferative response of total, CD4-depleted, and CD8-depleted lymphocytes suspensions to PHA was demonstrated. The level of expression of CD25 (IL-2 receptor) was similar in patients and controls before and after 24 h stimulation with PHA. We conclude that there is a disturbance in the functional properties of peripheral blood T cells that can contribute to the immunopathogenesis of SS. Meanwhile, the quantitative reduction of suppressor/inducer lymphocytes as defined by the CD4 2H4 phenotype can be precluded from a role in the development of such an autoimmune condition.

摘要

外周血中调节性T细胞亚群(包括最近描述的CD4辅助诱导细胞或抑制诱导细胞)平衡的变化可能在原发性干燥综合征(SS)的发病机制中起作用。采用直接免疫荧光法和流式细胞术对15例原发性SS患者和15例对照者的外周血淋巴细胞进行定量和分析。观察到SS患者循环CD4淋巴细胞百分比降低。患者循环CD4 + 2H4 +(抑制诱导细胞)、CD4 + 4B4 +(辅助诱导细胞)、CD2、CD3、CD8、CD8 + 2H4 +、CD8 + 4B4 +、CD25(IL - 2R)、CD19、CD16、CD57淋巴细胞的百分比无定量异常。患者中表达活化标志物HLA - DR的循环CD8淋巴细胞增加。通过PHA(植物血凝素)刺激评估外周血淋巴细胞的功能状态,随后通过放射性标记的胸腺嘧啶核苷摄取和CD25(白细胞介素 - 2受体)表达监测其增殖反应。结果显示,总淋巴细胞悬液、CD4去除的淋巴细胞悬液和CD8去除的淋巴细胞悬液对PHA的增殖反应降低。用PHA刺激24小时前后,患者和对照者CD25(IL - 2受体)的表达水平相似。我们得出结论,外周血T细胞的功能特性存在紊乱,这可能导致SS的免疫发病机制。同时,由CD4 2H4表型定义的抑制/诱导淋巴细胞的定量减少在这种自身免疫性疾病的发展中不起作用。

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