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Toll-like receptors: another player in the pathogenesis of the anti-phospholipid syndrome

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

MO Borghi

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

C Grossi

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

V Broggini

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

S Pierangeli

Division of Rheumatology. Department of Internal Medicine, University of Texas Medical Branch, Galveston, Texas, USA

PL Meroni

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

The anti-phospholipid syndrome (APS) is a systemic autoimmune disease characterized by an adaptive immune response against self phospholipid (PL)--binding proteins. Although APS is considered as an autoantibody-mediated disease, there is now evidence that anti-phospholipid antibodies (aPL) are necessary but not sufficient to trigger some of the clinical manifestations of the syndrome. For example, mediators of the innate immunity are recognized to be additional second hits able to induce the thrombotic events in the presence of aPL. Finally, environmental agents – in particular infectious ones – were reported to act as triggers for the production of autoantibodies cross-reacting with PL-binding proteins as well as inflammatory stimuli that potentiate the aPL thrombogenic effect. Altogether, these findings suggest a role for the innate immunity in APS pathogenesis. Toll-like receptors (TLR) are receptors that induce prompt inflammatory responses and mediate functional activation in immune effector cells. There is evidence that aPL, and in particular anti-β₂ glycoprotein I (β₂GPI) antibodies, may activate endothelial cells and monocytes through TLR-4-dependent signalling. Whether or not TLR may behave as surface receptors for β₂GPI is still matter of research. Drugs or molecules able to interfere with TLR involvement may represent new therapeutic approaches for APS.

Key Words: anti-phospholipid syndrome • beta2 glycoprotein I • innate immunity • thrombosis • toll-like receptors

Lupus, Vol. 17, No. 10, 938-943 (2008)
DOI: 10.1177/0961203308095140


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