Genetics of antiphospholipid syndrome.

被引：9

作者：

Horita T. ^{[1
]}

Merrill J.T. ^{[1
]}

机构：

[1] Clinical Pharmacology Research program, Oklahoma Medical Research Foundation, 825 NE 13th Street, Oklahoma City, 73104, OK

来源：

Current Rheumatology Reports | 2004年 / 6卷 / 6期

关键词：

Systemic Lupus Erythematosus; Systemic Lupus Erythematosus Patient; Human Leukocyte Antigen Class; Lupus Anticoagulant; Human Leukocyte Antigen Association;

D O I：

10.1007/s11926-004-0025-0

中图分类号：

学科分类号：

摘要：

Antiphospholipid syndrome (APS) is an autoimmune disease characterized by recurrent arterial or venous thrombosis or fetal loss and the presence of antiphospholipid antibodies (aPL). Genetic factors are thought to play a role in the susceptibility to APS. Similar to many other polygenic autoimmune diseases, human leukocyte antigen associations have been reported. The genetics of b(2)-glycoprotein I, one of the most representative target antigens of aPL, has been extensively studied. Additional genetic risk factors for the development of thrombosis in patients with aPL have also been discussed. However, the genes involved in APS have not been identified because antigen specificity of aPL and the pathophysiology of APS are highly heterogeneous and multifactorial. Genome-wide linkage analysis and larger cohort studies would lead to better understanding of the genes that might be involved in APS.

引用

页码：458 / 462

页数：4

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