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细胞因子在小鼠原发性抗磷脂综合征诱导中的假定作用。

The putative role of cytokines in the induction of primary anti-phospholipid syndrome in mice.

作者信息

Fishman P, Bakimer R, Blank M, Sredni D, Djaldetti M, Shoenfeld Y

机构信息

Hematology Research Unit, Golda Medical Centre, Hasharon Hospital, Petach Tiqva, Israel.

出版信息

Clin Exp Immunol. 1992 Nov;90(2):266-70. doi: 10.1111/j.1365-2249.1992.tb07940.x.

Abstract

Antiphospholipid syndrome (APLS) is characterized by thrombocytopenia, thromboembolic phenomena and recurrent fetal loss, associated with anti-cardiolipin antibodies (ACA) and/or lupus anticoagulant. The syndrome may be primary or may be associated with other conditions such as systemic lupus erythematosus (SLE). In this study we induced primary APLS following immunization of BALB/c mice with a human monoclonal ACA (H-3). Analysis of the cytokine profile of the mice with experimental APLS indicated low production of IL-2, IL-3 and granulocyte-macrophage colony-stimulating factor (GM-CSF) by concanavalin A (Con A)-stimulated splenocytes of H-3 immunized mice. It seems that the low levels of IL-3 and GM-CSF have a potential role in the fetal loss of the APLS. Whatever the mechanism of IL-3 and GM-CSF in preventing fetal loss, these results may have therapeutic bearing on the reproductive outcome in women and other species with APLS.

摘要

抗磷脂综合征(APLS)的特征为血小板减少、血栓栓塞现象和反复流产,与抗心磷脂抗体(ACA)和/或狼疮抗凝物相关。该综合征可以是原发性的,也可能与其他病症如系统性红斑狼疮(SLE)有关。在本研究中,我们用一种人单克隆ACA(H-3)免疫BALB/c小鼠,诱导出原发性APLS。对实验性APLS小鼠的细胞因子谱分析表明,用H-3免疫的小鼠经刀豆蛋白A(Con A)刺激的脾细胞产生的白细胞介素-2(IL-2)、白细胞介素-3(IL-3)和粒细胞巨噬细胞集落刺激因子(GM-CSF)水平较低。似乎IL-3和GM-CSF水平较低在APLS的流产中具有潜在作用。无论IL-3和GM-CSF预防流产的机制如何,这些结果可能对患有APLS的女性和其他物种的生殖结局具有治疗意义。

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