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Endothelium and the brain in CNS lupus

Allergy and Clinical Immunology Unit, Department of Internal Medicine, University of Milan, IRCCS Istituto Auxologico Italiano, Milan, Italy, pierluigi.meroni{at}unimit.it

A Tincani

Rheumatology, Allergy and Clinical Immunology, Spedali Civili, Brescia, Italy

N Sepp

Department of Dermatology, University of Innsbruck, Austria

E Raschi

Allergy and Clinical Immunology Unit, Department of Internal Medicine, University of Milan, IRCCS Istituto Auxologico Italiano, Milan, Italy

C Testoni

Allergy and Clinical Immunology Unit, Department of Internal Medicine, University of Milan, IRCCS Istituto Auxologico Italiano, Milan, Italy

E Corsini

IRCCS Istituto Neurologico Besta, Milan, Italy

I Cavazzana

Rheumatology, Allergy and Clinical Immunology, Spedali Civili, Brescia, Italy

S Pellegrini

Allergy and Clinical Immunology Unit, Department of Internal Medicine, University of Milan, IRCCS Istituto Auxologico Italiano, Milan, Italy

A Salmaggi

IRCCS Istituto Neurologico Besta, Milan, Italy

Central nervous system (CNS) involvement in systemic lupus erythematosus (SLE) is common and results in different clinical manifestations. Several pathogenic mechanisms have been suggested to play a rolein determiningsuch a varietyof clinicalsymptoms.The thrombophilicstateassociatedto the presence of antiphospholipidantibodies has been suggested to be responsible for a noninflammatory vasculopathywhichcauses clear ischaemiceventsas well as alterationsof the cerebralmicrocirculation that are likely associated to seizures, cognitive dysfunction or psychosis. Although less frequent, a true vasculitic process affecting cerebral circulation has also been reported. In both cases, brain endothelium does represent the target of the pathogenic mechanisms. Brain endothelial cells display peculiar functional and phenotypical characteristics in comparison with endothelial cells from other anatomical districts, raising the possibility that this might be the reason for its susceptibility in lupus disease. We review and present data suggesting that a higher and firmer expression of beta 2 glycoprotein I on endothelialcell membranes can be responsiblefor a selective damage/activation by circulating anti-beta 2 glycoprotein I, and that antiendothelial cell antibodies crossreact with brain endothelium and in some cases, specifically bind brain endothelial cells only in lupus patients with central nervous involvement.

Key Words: autoantibodies • CNS • endothelium • SLE • thrombosis

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