ABSTRACT
Anti-cardiolipin (aCL) antibodies in human systemic lupus erythematosus (SLE) and related conditions are closely associated with serious clinical complications consisting of venous and arterial thrombosis, mid-pregnancy fetal death, and thrombocytopenia (“antiphospholipid syndrome”). Inhibition studies demonstrated that, in contrast to previous reports of murine monoclonal IgM antibodies crossreacting with polynucleotides and phospholipids, there was no cross-reactivity between polyclonal IgG anti-DNA and aCL antibodies. Studies in human SLE have shown that IgG anti-DNA are mostly of the IgGl and IgG3 (complement fixing) subclasses, whereas IgG aCL are distributed among all four IgG subclasses with higher contributions of IgG2 and IgG4 (the weak/noncomplement fixing subclasses). Detection of high levels of polyclonal IgG aCL with phospholipid specificities virtually identical to those observed in human SLE, as well as the absence of crossreactivity between anti-DNA and aCL antibodies, raised the question as to whether MRL/lpr mice suffer from aPL-associated clinical complications.
