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在未接触过的小鼠中诱导实验性原发性和继发性抗磷脂综合征。

Induction of experimental primary and secondary antiphospholipid syndromes in naive mice.

作者信息

Shoenfeld Y

机构信息

Department of Medicine, Sheba Medical Center, Tel-Hashomer, Israel.

出版信息

Am J Reprod Immunol. 1992 Oct-Dec;28(3-4):219-21. doi: 10.1111/j.1600-0897.1992.tb00796.x.

Abstract

In the current series of experimental studies we show that anticardiolipin antibodies (ACA) are pathogenic: Infusion of serum ACA to the tail vein of naive mice induces experimental antiphospholipid syndrome (APLS) characterized by thrombocytopenia, prolonged aPTT, and recurrent fetal resorptions. Similar experimental APLS is induced by active immunization with serum as well as with natural human monoclonal ACA. APLS is also associated with low fecundity rate. The experimental APLS models were employed to demonstrate the efficacy of aspirin, low molecular heparin, and interleukin-3 preventing recurrent fetal loss. In another experiment, immunization with human monoclonal anti-DNA antibody was followed by the induction of APLS secondary to experimental systemic lupus erythematosus (SLE). In all studies, IgGs were found to be more pathogenic than IgMs ACA. These studies confirm the autoimmune nature of APLS.

摘要

在当前这一系列实验研究中,我们表明抗心磷脂抗体(ACA)具有致病性:将血清ACA注入未接触过抗原的小鼠尾静脉会诱发实验性抗磷脂综合征(APLS),其特征为血小板减少、活化部分凝血活酶时间(aPTT)延长以及反复出现胎儿吸收。用血清以及天然人源单克隆ACA进行主动免疫也会诱发类似的实验性APLS。APLS还与低生育率相关。采用实验性APLS模型来证明阿司匹林、低分子肝素和白细胞介素-3预防反复性胎儿丢失的效果。在另一项实验中,用人源单克隆抗DNA抗体进行免疫后,继发于实验性系统性红斑狼疮(SLE)而诱发了APLS。在所有研究中,发现IgG型ACA比IgM型ACA更具致病性。这些研究证实了APLS的自身免疫性质。

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