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原发性干燥综合征患者外周血中1型细胞因子分泌细胞频率的改变。

Altered frequency of type 1 cytokine secreting cells in the peripheral blood of patients with primary Sjögren's syndrome.

作者信息

Hagiwara E, Pando J, Ishigatsubo Y, Klinman D M

机构信息

Section of Retroviral Immunology, Center for Biologics Evaluation and Research, US Food and Drug Administration, Bethesda, MD, USA.

出版信息

J Rheumatol. 1998 Jan;25(1):89-93.

PMID:9458209
Abstract

OBJECTIVE

An imbalance in immunoregulatory cytokines may contribute to the etiopathogenesis of Sjogren's syndrome (SS). We investigated systemic abnormalities in cytokine production in the peripheral blood in patients with SS.

METHODS

ELISPOT assays were used to detect and enumerate cells spontaneously secreting interleukin 2 (IL-2), IL-6, IL-10, and interferon-gamma (IFN-gamma) in freshly isolated peripheral blood mononuclear cells from 20 patients with SS and 20 healthy controls.

RESULTS

The number of cells spontaneously secreting type 1 cytokines IL-2 and IFN-gamma was decreased in the peripheral blood of patients with SS compared to controls. There was no change observed in the number of cells spontaneously secreting IL-6 and IL-10. Cells spontaneously secreting IL-4 were too rare in peripheral blood to evaluate, although cells capable of secreting IL-4 in response to phytohemagglutinin did not differ from controls. Patients with severe extraglandular symptoms (such as vasculitis) had a significantly lower frequency of IFN-gamma secreting cells in their peripheral blood than those without extraglandular involvement.

CONCLUSION

These results suggest that decreased type 1 cytokine production may contribute to or reflect the pathogenesis of SS.

摘要

目的

免疫调节细胞因子失衡可能参与干燥综合征(SS)的发病机制。我们研究了SS患者外周血中细胞因子产生的全身异常情况。

方法

采用酶联免疫斑点试验(ELISPOT)检测并计数20例SS患者和20例健康对照者新鲜分离的外周血单个核细胞中自发分泌白细胞介素2(IL-2)、IL-6、IL-10和干扰素-γ(IFN-γ)的细胞。

结果

与对照组相比,SS患者外周血中自发分泌1型细胞因子IL-2和IFN-γ的细胞数量减少。自发分泌IL-6和IL-10的细胞数量未观察到变化。外周血中自发分泌IL-4的细胞过于稀少,无法评估,尽管对植物血凝素产生反应而分泌IL-4的细胞与对照组无差异。有严重腺外症状(如血管炎)的患者外周血中分泌IFN-γ的细胞频率明显低于无腺外受累的患者。

结论

这些结果表明,1型细胞因子产生减少可能参与或反映了SS的发病机制。

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