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The molecular basis of antiphospholipid syndromeDepartment of Medicine, Morehouse School of Medicine, Atlanta, GA, USA, aghara{at}pol.net
Division of Rheumatology, School of Medicine, Louisiana State University, Louisiana, USA
Department of Microbiology, Biochemistry and Immunology, Morehouse School of Medicine, Atlanta, GA, USA We herein review evidence that the phospholipid-binding protein ß2 glycoprotein-1 (ß2 GPI) is a causativeautoantigenin APS. Recent work suggeststhat the molecular regions in ß2 GPI that facilitate autoimmunization are those that promote binding to negatively charged phospholipids by means of strong positive (anionic) charge and hydrophobicity. Although many common infections can cause antiphospholipidantibodies to be produced in humans, such postinfectious aPL are rarely associated with thromboses or pregnancy morbidity, the central features of antiphospholipid syndrome (APS). We propose that the causes of APS include those infectious agents that mimic the above molecular domains in ß2 GPI. In peoplewho are susceptibleto APS, tolerance to self-ß2 GPI and phospholipidsis likely to be broken by foreign bacterial or viral proteins that contain such ß2 GPI-like epitopes.
Lupus, Vol. 12, No. 8,
579-583 (2003) This article has been cited by other articles:
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