Antiphospholipid syndrome's genetic and epigenetic aspects

被引：24

作者：

Iuliano, Annamaria ^{[1
]}

Galeazzi, Mauro ^{[2
]}

Sebastiani, Gian Domenico ^{[1
]}

机构：

[1] Azienda Osped San Camillo Forlanini, Rheumatol Unit, Rome, Italy

[2] Univ Siena, Inst Rheumatol, Siena, Italy

来源：

AUTOIMMUNITY REVIEWS | 2019年 / 18卷 / 09期

关键词：

Antiphospholipid syndrome; Anticardiolipin antibodies; Anti-beta2glycoprotein I antibodies; Lupus anticoagulant; HLA; MHC; microRNA; Thrombofilic hereditary factors; SYSTEMIC-LUPUS-ERYTHEMATOSUS; CLASS-II ALLELES; HLA-DR ANTIGENS; ANTICARDIOLIPIN ANTIBODIES; BETA(2)-GLYCOPROTEIN I; CARDIOLIPIN ANTIBODIES; RHEUMATIC-DISEASES; EUROPEAN PATIENTS; LARGE SERIES; ASSOCIATION;

D O I：

10.1016/j.autrev.2019.102352

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Studies on last genetic and epigenetic predisposition to APS are summarized. It is well known that genetic predisposition is in HLA system (DR4 and DRw53) and that lupus anticoagulant (LA) and anticardiolipin antibodies (aCL) are both associated with the same HLA antigens. Other genes, outside the MHC, give their contribution to the development of this autoimmune syndrome, such as IRF5, STAT4 and those related to inherited thrombophilia - factor V Leiden and G20210A prothrombin polymorphisms. Finally, post-transcriptional modifications of anti-beta2GPI antibodies could be implicated too. The most important discovery of last years is that altered microRNAs' expression is linked to autoimmunity, thrombosis, early atherosclerosis, and oxidative stress in APS.

引用

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