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病毒肽与急性早幼粒细胞白血病诱导的新进展。

New developments in viral peptides and APL induction.

作者信息

Gharavi A E, Pierangeli S S, Harris E N

机构信息

Department of Medicine, Morehouse School of Medicine, Atlanta, GA 30310-1495, USA.

出版信息

J Autoimmun. 2000 Sep;15(2):227-30. doi: 10.1006/jaut.2000.0403.

Abstract

The associations of antiphospholipid antibodies (aPL) with thrombosis and fetal death are well recognized, but the mechanism(s) that induce their production are not. We demonstrated induction of pathogenic aPL antibodies by immunization with foreign beta(2)-GPI, or synthetic peptides representing the PL-binding site of the beta(2)-GPI. These antibodies caused intrauterine fetal death and transverse myelopathy due to spinal cord infarction in mice, and activated endothelial cells in vitro. We also introduced aPL in mice by immunization with PL-binding viral peptides and observed their pathogenic effects. This study demonstrated that pathogenic effects of aPL antibodies induced by immunization with a human CMV-derived PL-binding synthetic peptide. We hypothesize that in APS patients aPL is induced by beta(2)-GPL-like PL-binding products of human common bacteria or viruses.

摘要

抗磷脂抗体(aPL)与血栓形成和胎儿死亡之间的关联已得到充分认识,但其产生机制尚不清楚。我们通过用外源性β2 -糖蛋白I(β2 -GPI)或代表β2 -GPI磷脂结合位点的合成肽进行免疫接种,证明了致病性aPL抗体的诱导。这些抗体导致小鼠宫内胎儿死亡和因脊髓梗死引起的横贯性脊髓病,并在体外激活内皮细胞。我们还通过用磷脂结合病毒肽免疫接种在小鼠中引入aPL,并观察到它们的致病作用。本研究表明,用人巨细胞病毒衍生的磷脂结合合成肽免疫接种诱导的aPL抗体具有致病作用。我们推测,在抗磷脂综合征(APS)患者中,aPL是由人类常见细菌或病毒的β2 -GPL样磷脂结合产物诱导产生的。

相似文献

1
New developments in viral peptides and APL induction.
J Autoimmun. 2000 Sep;15(2):227-30. doi: 10.1006/jaut.2000.0403.
2
Origin of antiphospholipid antibodies: induction of aPL by viral peptides.
Lupus. 1998;7 Suppl 2:S52-4. doi: 10.1177/096120339800700213.

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The antiphospholipid syndrome and infection.
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