Journal of Clinical Immunology

, Volume 15, Supplement 6, pp S86–S100

The antiphospholipid-protein syndrome

Authors

  • Douglas B. Cines
    • Department of Pathology and Laboratory Medicine, 7 Founders PavilionHospital of the University of Pennsylvania
  • Keith R. McCrae
    • Sol Sherry Thrombosis Research CenterTemple University School of Medicine
The Role of Superantigens in Disease and Animal Models as Instructional Paradigms of Human Disease

DOI: 10.1007/BF01540898

Cite this article as:
Cines, D.B. & McCrae, K.R. J Clin Immunol (1995) 15: S86. doi:10.1007/BF01540898

Abstract

The pathogenesis of the antiphospholipid syndrome remains uncertain. Antibodies that react with phospholipids may not be directly responsible for cellular injury, but may be part of the immune network through which autoantibodies with pathogenic potential are generated. The latter may recognize proteins such asβ2-glycoprotein I that form complexes with phospholipids, proteins whose functions depend upon interaction with phospholipids such as protein C and its cofactors, altered lipoproteins such as oxidized low-density lipoproteins, or other molecules that share only antigenic similarity. Thus, a spectrum of autoantibodies that recognize different lipid-protein complexes may develop in these patients and contribute to the observed clinical heterogeneity of the syndrome. Current techniques do not permit identification of the subset of patients with antiphospholipid antibodies at risk for thrombosis or abortion and there are no prospective, controlled trials addressing the prophylaxis or treatment of affected individuals. Identification of the cellular targets of antibodies to lipid-protein moieties is needed to identify patients at risk for these complications and as a means to monitor therapy.

Key words

Antiphospholipid antibodiesthrombosisabortionautoantibodies
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Copyright information

© Plenum Publishing Corporation 1995