Tissue factor expression on monocytes induced by anti-phospholipid antibodies as a strong risk factor for thromboembolic complications in SLE patients

被引:26
作者
Nojima, Junzo [1 ]
Masuda, Yumiko
Iwatani, Yoshinori
Suehisa, Etsuji
Futsukaichi, Yoshiaki
Kuratsune, Hirohiko
Watanabe, Yasuyoshi
Takano, Toru
Hidaka, Yoh
Kanakura, Yuzuru
机构
[1] Osaka Univ Hosp, Clin Invest Lab, Osaka 5650871, Japan
[2] Osaka Univ, Grad Sch Med, Course Hlth Sci, Div Biomed Informat, Osaka, Japan
[3] Kansai Univ Welf Sci, Fac Hlth Sci Welf, Dept Hlth Sci, Osaka, Japan
[4] Osaka City Univ, Grad Sch Med, Dept Physiol, Abeno Ku, Osaka 558, Japan
[5] Osaka Univ, Grad Sch Med, Dept Hematol & Oncol, Osaka, Japan
关键词
systemic lupus erythematosus; anti-phospholipid syndrome; monocyte; tissue factor; anti-cardiolipin antibodies; thromboembolic complications; enzyme-linked immunosorbent assay; flow cytometry;
D O I
10.1016/j.bbrc.2007.10.173
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Our aim was to clarify the role of anti-phospholipid antibodies in the pathogenesis of monocyte tissue factor (TF) expression and thromboembolic complications (TE) in patients with SLE. We examined cell surface expression of TF on monocytes in 93 SLE patients. Monocyte TF expression was significantly higher in SLE patients who had TE than in other SLE patients, and confirmed that the high expression of monocyte TF was a strong risk factor for TE. Furthermore, the presence of anti-cardiolipin/beta 2-glycoprotein I antibodies (anti-CL/beta 2-GPI) was strongly associated with the high expression of monocyte TF. We therefore studied the in vitro effect of IgG anti-CL/beta 2-GPI on lipopolysaccharide (LPS)-induced expression of TF on monocytes in healthy peripheral blood and found that purified IgG containing anti-CL/beta 2-GPI significantly enhanced LPS-induced monocyte TF expression. These results suggest that anti-CL/beta 2-GPI cause persistently high TF expression on monocyte, which may contribute to the risk of thromboembolic events in SLE patients. (c) 2007 Elsevier Inc. All rights reserved.
引用
收藏
页码:195 / 200
页数:6
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