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* Department of Medicine, Division of Rheumatology, Center for Rheumatic Diseases, Kangnam St. Mary’s Hospital, and Research Institute of Immunobiology, Catholic Research Institutes of Medical Sciences, Catholic University of Korea, Seoul, Korea; and
Department of Medicine, University of California School of Medicine, Los Angeles, CA 90095
The presence of antiphospholipid Ab is associated with increased
risk of thrombosis. The monocyte-endothelial cell interaction has been
suggested to play a key role at the site of vascular injury during
thrombosis. Therefore, we tested the effect of anticardiolipin Abs
(aCL) on the production of monocyte chemoattractant protein-1 (MCP-1)
in HUVEC. We found that monoclonal aCL as well as IgG fractions from
patients with antiphospholipid syndrome (APS-IgG) could induce the
production of MCP-1 in HUVEC. The ability of IgG aCL to induce MCP-1
production could be abrogated by preabsorption with cardiolipin
liposomes. Simultaneous addition of either monoclonal aCL or APS-IgG
with IL-1
resulted in synergistic increase in MCP-1 production,
whereas the addition of control IgG lacking aCL activity did not alter
IL-1-induced levels of MCP-1. MCP-1 mRNA expression was also
up-regulated when HUVEC were incubated with either APS-IgG or
monoclonal aCL, and down-regulated by the treatment of dexamethasone.
In addition, we found that serum levels of MCP-1 in 76 systemic lupus
erythematosus patients correlated well with the titers of IgG aCL.
Collectively, these results indicate that aCL could promote endothelial
cell-monocyte cross-talk by enhancing the endothelial production of
MCP-1, thereby shifting the hemostatic balance toward the prothrombotic
state of APS.
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