SERUM ANTI-BETA(2)-GLYCOPROTEIN-I ANTIBODIES FROM PATIENTS WITH ANTIPHOSPHOLIPID ANTIBODY SYNDROME BIND CENTRAL-NERVOUS-SYSTEM CELLS

Sera from 20 patients with antiphospholipid syndrome (APS), primary or secondary to systemic lupus erythematosus (SLE), or with SLE, were as sayed by immunoblot analysis for anti-beta(2)-glycoprotein I antibodie s (a beta(2)-GPI), and by indirect immunofluorescence (IIF) technique for reactivity with astrocyte and neuron cell lines and with histologi cal sections of human brain biopsies and monkey cerebellum. Six sera f rom healthy donors were studied as a control. Eleven out of the 20 pat ient sera contained a beta(2)-GPI and were immunoreactive with astrocy tes and neurons, both in culture and in the histological sections, and with the endotheliocytes of the microvessels present in the histologi cal sections. Cell localization and the pattern of immune reaction wer e similar to those obtained with a monoclonal antibody a beta(2)-GPI. Eight of the remaining patient sera, found a beta(2)-GPI(-), did not r eact with the nervous substrates (and the control sera), while one exh ibited immunoreactivity analogous to the a beta(2)-GPI(+) sera. The in terference of anticardiolipin antibodies (aCL) in the immunoreactivity with the nervous substrates was excluded since aCL were present in al l patient sera and no immune reaction was observed in the histological sections incubated with a monoclonal aCL. Therefore, the binding of a beta(2)-GPI from patients to cells of the central nervous system (CNS ) occurs independently from aCL. This issue may be relevant to further evaluate the potential pathogenetic role of a beta(2)-GPI in the CNS damage of APS-like conditions. (C) 1998 Academic Press