载脂蛋白H在抗磷脂抗体综合症中作用的细胞与分子机理

Antiphospholipid syndromes（APS）are serious autoimmune diseases. b2-glycoprotein I （b2-GPI）or apolipoprotein H （ApoH）. In recent years, interest in b2GPI increased dramatically because it has been proposed to be most clinically relevant in patients with anti-phospholipid syndrome (APS). .The present study are shown bellow:.1．To investigate polymorphisms of human serum b2-glycoprotein I in about 500 healthy Chinese and 52 APS positive by isoelectroric focusing analysis. It indicated that although for APS patient, the ApoH allele frequencities do not significantly alter, some abnormal changes of serum ApoH in gene expression and molecular structure may occur, resulting in the alteration of antigenicity..2．Anticardiolipid antibody (ACA) in APS patients' serum displayed remarkable anti-b2-GPI activity. It is proposed that the ACA-targeted antigenicity was involved in alterated b2-GPI, which might cause 'antigen-drive' immunoreaction. .3. For first time indicated that there was a Fc-binding factor in APS patients' serum, which was identified with anti-b2-GPI antibody as well as ACA..4. For first time showed that the plasma soluble protein b2-glycoprotein is a cofactor or activator of tPA to significantly augment the tPA-dependent plasminogen activation. The specific ability of b2GP can be inhibited markedly by anti-b2GP antibody and was b2GPI dose-responsive, and that the further activation by plasmin may provide a nevol positive feedback mechanism of intrinsic fibrinolysis.The complex prothrombosis and anti-coagulation in APS patient' vascular system was explained in view of this novel activation pathway of tPA-dependent plasminogen system.5. To demonstrate the importance of the formation of b2-GPI-antib2-GPI antibody-annexin II-anti annexin II antibody complex in the cellular mechanism of APS. To investigate bioenergics in apoptosis, the relation between BcL-2 gene and telomerase activities in apoptosis, the anti-apoptosis of collagen..

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