ANTIENDOTHELIAL CELL ANTIBODIES IN PRIMARY ANTIPHOSPHOLIPID SYNDROME AND SLE - PATTERNS OF REACTIVITY WITH MEMBRANE-ANTIGENS ON MICROVASCULAR AND UMBILICAL VENOUS CELL-MEMBRANES

Citation
Mb. Hill et al., ANTIENDOTHELIAL CELL ANTIBODIES IN PRIMARY ANTIPHOSPHOLIPID SYNDROME AND SLE - PATTERNS OF REACTIVITY WITH MEMBRANE-ANTIGENS ON MICROVASCULAR AND UMBILICAL VENOUS CELL-MEMBRANES, British Journal of Haematology, 103(2), 1998, pp. 416-421
Citations number
25
Categorie Soggetti
Hematology
ISSN journal
00071048
Volume
103
Issue
2
Year of publication
1998
Pages
416 - 421
Database
ISI
SICI code
0007-1048(1998)103:2<416:ACAIPA>2.0.ZU;2-M
Abstract
Although there has been recent emphasis on autoantibodies to epitopes on beta-2-glycoprotein I and prothrombin in the pathogenesis of antiph ospholipid syndrome (APS), antibodies other than those directed toward epitopes on phospholipid binding proteins are present. These include those reactive with antigens on platelet membrane glycoproteins, and w ith vascular endothelial cell membrane. As the pathogenesis of the thr ombotic manifestations of APS remains unexplained, further characteriz ation of these antibodies may be informative. We have confirmed anti-e ndothelial cell binding to a range of cell membrane antigene in system ic lupus erythematosus (SLE) and primary APS. Furthermore, differences in both the pattern of antibody binding and band intensity between hu man umbilical vein (HUVEC) and human microvascular endothelial cells ( HMEC-1) were demonstrated. Of 17 primary APS sera, antibody binding to HUVEC cell membranes was found in nine and to HMEC-1 membranes in sev en. Binding at 72-79 kD was confined to HUVEC. In 32 SLE sera, binding to HUVEC and HMEC-1 membranes was detected in 17 and 22 respectively, binding at 135-155 kD being confined to HMEC-1. These results are con sistent with the phenotypic variation in endothelial cells of differen t origins and confirm the frequent presence of autoantibodies reactive with vascular endothelium in both SLE and PAPS. Whether these antibod ies could be involved in the pathogenesis of thrombosis, through induc tion of endothelial cell apoptosis or damage, remains to be determined .