Anti-β2-glycoprotein I antibodies bind to central nervous system

被引:58
作者
Caronti, B
Pittoni, V
Palladini, G
Valesini, G [1 ]
机构
[1] Univ La Sapienza, Allergol & Immunol Clin 3, Rome, Italy
[2] Univ La Sapienza, Dipartimento Sci Neurol, Rome, Italy
关键词
anti-beta(2)-glycoprotein antibodies; central nervous system; anti-phospholipid syndrome;
D O I
10.1016/S0022-510X(98)00027-6
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Anti-beta(2)-GPI antibodies (a beta(2)-GPI) were found in serum from patients with anti-phospholipid syndrome (APS) and/or systemic lupus erythematosus (SLE). Since a beta(2)-GPI are often found in patients with anti-cardiolipin antibodies (aCL), their role in thrombosis as well as other central nervous system (CNS) manifestations in APS is unclear. We, therefore, investigated whether affinity-purified a beta(2)-GPI bind the CNS. Astrocyte and neuron cell lines and histological sections were used as CNS substrates. Indirect immunofluorescence and/or streptavidin-biotin-peroxidase techniques revealed that astrocytes, neurons and vascular endothelium were bound by purified a beta(2)-GPI (mouse monoclonal, rabbit polyclonal, human serum Ig a beta(2)-GPI). This suggests a potential role for a beta(2)-GPI in the CNS damage, as a beta(2)-GPI might contribute to CNS pathology by either a direct interaction with astrocytes and neurons or an interaction with cerebral vascular endothelial cells. CNS immunoreaction was also demonstrated using six a beta(2)-GPI-positive sera from patients (four with neurological manifestations). No binding to CNS was seen using a beta(2)-GPI-negative sera, i.e. five from SLE patients (two with CNS involvement) and six healthy donors, or a monoclonal aCL without a beta(2)-GPI immunoreactivity. Thus, the CNS reactivity by the a beta(2)-GPI-positive sera appears specifically due to a beta(2)-GPI and independent from aCL. Because of the presence of aCL in all patient sera, and the CNS involvement in three control patients, it is not possible to attribute a direct role for a beta(2)-GPI in neurological diseases in this study. (C) 1998 Elsevier Science B.V.
引用
收藏
页码:211 / 219
页数:9
相关论文
共 51 条
[11]  
CUSIMANO G, 1990, ACTA NEUROL SCAND, V81, P215
[12]  
DELPAPA N, 1995, CLIN EXP RHEUMATOL, V13, P179
[13]  
DERKSEN RHWM, 1994, NETH J MED, V45, P257
[14]   SPECIAL REPORT - THE COMPLEXITY OF ENDOTHELIAL-CELLS [J].
FAJARDO, LF .
AMERICAN JOURNAL OF CLINICAL PATHOLOGY, 1989, 92 (02) :241-250
[15]   NEUROPSYCHIATRIC LUPUS-ERYTHEMATOSUS, CEREBRAL INFARCTIONS, AND ANTICARDIOLIPIN ANTIBODIES [J].
FIELDS, RA ;
SIBBITT, WL ;
TOUBBEH, H ;
BANKHURST, AD .
ANNALS OF THE RHEUMATIC DISEASES, 1990, 49 (02) :114-117
[16]   ANTICARDIOLIPIN ANTIBODIES (ACA) DIRECTED NOT TO CARDIOLIPIN BUT TO A PLASMA-PROTEIN COFACTOR [J].
GALLI, M ;
COMFURIUS, P ;
MAASSEN, C ;
HEMKER, HC ;
DEBAETS, MH ;
VANBREDAVRIESMAN, PJC ;
BARBUI, T ;
ZWAAL, RFA ;
BEVERS, EM .
LANCET, 1990, 335 (8705) :1544-1547
[17]   INDUCTION OF ANTIPHOSPHOLIPID AUTOANTIBODIES BY IMMUNIZATION WITH BETA-2 GLYCOPROTEIN-I (APOLIPOPROTEIN-H) [J].
GHARAVI, AE ;
SAMMARITANO, LR ;
WEN, JY ;
ELKON, KB .
JOURNAL OF CLINICAL INVESTIGATION, 1992, 90 (03) :1105-1109
[18]  
GHARAVI AE, 1993, J LAB CLIN MED, V122, P426
[19]   TRANSIENT HTLV-1 INFECTION OF A HUMAN GLIOMA CELL-LINE FOLLOWING CELL-FREE EXPOSURE [J].
GRAZIANI, G ;
FARAONI, I ;
ZHANG, J ;
CARONTI, B ;
LAURO, G ;
BONMASSAR, E ;
MACCHI, B .
VIROLOGY, 1993, 197 (02) :767-769
[20]  
HARDY RR, 1986, HDB EXPT IMMUNOLOGY, V13, P1