期刊
LUPUS
卷 13, 期 1, 页码 17-23出版社
SAGE PUBLICATIONS LTD
DOI: 10.1191/0961203304lu484oa
关键词
anticardiolipin antibodies; antiphospholipid antibodies; antiphospholipid syndrome; CMV; molecular mimicry; pregnancy loss
类别
资金
- NATIONAL CENTER FOR RESEARCH RESOURCES [G12RR003034] Funding Source: NIH RePORTER
- NCRR NIH HHS [G12-RR03034] Funding Source: Medline
- NIGMS NIH HHS [502 GM 08248] Funding Source: Medline
Immunization of mice with beta(2) glycoprotein I (beta(2)GPI) and also with GDKV a synthetic peptide representing the phospholipid (PL)-binding site of beta(2)GPI, induced pathogenic aPL antibodies that bind and activate endothelial cells, enhanced thrombus formation and caused fetal death in pregnant mice. TIFI is a PL-binding peptide spanning the Thr101-Thr120 of ulb0-hcmva from human cytomegalovirus (CMV), which shares structural similarity with the PL-binding site Of beta(2)GPI. Immunization with this peptide induced pathogenic aPL and anti-beta(2)GPI antibodies in mice. These antibodies activated endothelial cells and enhanced thrombus formation in vivo, but whether these antibodies cause fetal death in mice is not known. The objective of this study was to examine the effects of these antibodies on pregnancy outcome in mice. Two groups of pregnant BALB/c mice were injected with either hybridoma supernatant containing D3/AC10, a CMV - peptide-induced monoclonal aPL, at days four, eight and 12 of the pregnancy, 100 mug per mouse (study group) or with culture media alone (control group). The litter size was significantly smaller in the study group (4.80 +/- 1.15 versus 7.28 +/- 0.18, t = - 2.5265 P < 0.03). In conclusion, aPL induced by CMV peptides may have pathogenic properties similar to human autoinumune aPL. These findings further support the hypothesis that at least in some patients with APS, pathogenic aPL antibodies may be generated by immunization with CMV products during incidental exposure to the virus via a molecular mimicry mechanism.
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