RELATIONSHIP BETWEEN ANTIPHOSPHOLIPID AND ANTIENDOTHELIAL CELL ANTIBODIES .3. BETA-2 GLYCOPROTEIN-I MEDIATES THE ANTIBODY-BINDING TO ENDOTHELIAL MEMBRANES AND INDUCES THE EXPRESSION OF ADHESION MOLECULES
N. Delpapa et al., RELATIONSHIP BETWEEN ANTIPHOSPHOLIPID AND ANTIENDOTHELIAL CELL ANTIBODIES .3. BETA-2 GLYCOPROTEIN-I MEDIATES THE ANTIBODY-BINDING TO ENDOTHELIAL MEMBRANES AND INDUCES THE EXPRESSION OF ADHESION MOLECULES, Clinical and experimental rheumatology, 13(2), 1995, pp. 179-185
Objective: To investigate the role of antibodies reacting with beta 2
glycoprotein I(beta 2GPI) in the antiendothelial cell binding activity
present in sera from patients with the anti-phospholipid syndrome. Me
thods: Sera positive for anti-phospholipid, anti-endothelial and anti-
beta 2 GPI antibodies were studied for their binding activity on endot
helial monolayers cultured in the presence or absence of media contain
ing bovine serum as a source of beta 2 GPI. Anti-endothelial activity
was also evaluated on endothelial cells cultured without serum and sup
plemented with exogenous human purified beta 2 GPI. Affinity purified
anti-beta 2 GPI antibodies were investigated under the same experiment
al conditions Finally the effect of the incubation of these affinity p
urified fractions on the expression of adhesion molecules (ELAM-1) was
studied. Results: The reactivity of the sera decreased on endothelial
cells incubated in serum-free medium, while endothelial cell binding
was restored in a dose dependent manner after the addition of exogenou
s purified human beta 2 GPI. Affinity purified anti-beta 2 GPI antibod
ies obtained from the same sera retained their endothelial cell bindin
g and were able to activate endothelial cells by inducing the ex novo
surface expression of adhesion molecules (ELAM-1). Conclusions: These
findings indicate that the close association between anti-endothelial
and anti-phospholipid antibodies is sustained by antibodies which reco
gnize beta 2 GPI adhering to the endothelial cells, and can promote th
eir activation.