Antiphospholipid syndrome infectious origin

被引:97
作者
Blank, M
Asherson, RA
Cervera, R
Shoenfeld, Y [1 ]
机构
[1] Chaim Sheba Med Ctr, Dept Med B, IL-52621 Tel Hashomer, Israel
[2] Chaim Sheba Med Ctr, Ctr Autoimmune Dis, IL-52621 Tel Hashomer, Israel
[3] Tel Aviv Univ, Sackler Fac Med, IL-69978 Tel Aviv, Israel
[4] Univ Cape Town, Sch Med, Rheumat Dis Unit, ZA-7925 Cape Town, South Africa
[5] Hosp Clin Barcelona, Inst Clin Infecc & Immunol, Dept Autoimmune Dis, Barcelona, Catalonia, Spain
关键词
antiphospholipid syndrome; beta; 2-glycoprotein-I; infection; molecular mimicry;
D O I
10.1023/B:JOCI.0000018058.28764.ce
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Antiphospholipid syndrome (APS) is characterized by the presence of pathogenic autoantibodies against beta2-glycoprotein-I (beta2GPI). The factors causing production of anti-beta2GPI remain unidentified, but an association with infectious agents has been reported. Studies on experimental APS models proved that molecular mimicry between beta2GPI-related synthetic peptides and structures within bacteria, viruses, tetanus toxoid, and CMV are a cause for experimental APS. Any explanation of how microbial infections might set off APS must take into account the observation that all individuals appear to harbor potentially autoreactive lymphocytes, as well as natural antiphospholipid antibodies, but that these cells or antibodies remain innocuous unless somehow activated. Herein, we discuss the association of antiphospholipid antibodies in the infectious state, molecular mimicry as a proposed cause for development of APS, and the contribution of the database to this topic.
引用
收藏
页码:12 / 23
页数:12
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