Animal models of the antiphospholipid syndrome


RADWAY-BRIGHT E., Inanc M., ISENBERG D.

RHEUMATOLOGY, vol.38, no.7, pp.591-601, 1999 (Peer-Reviewed Journal) identifier identifier identifier

  • Publication Type: Article / Review
  • Volume: 38 Issue: 7
  • Publication Date: 1999
  • Doi Number: 10.1093/rheumatology/38.7.591
  • Journal Name: RHEUMATOLOGY
  • Journal Indexes: Science Citation Index Expanded, Scopus
  • Page Numbers: pp.591-601
  • Keywords: animal model, antiphospholipid syndrome, antiphospholipid antibodies, beta 2-glycoprotein I, treatment, SYSTEMIC LUPUS-ERYTHEMATOSUS, POLYCLONAL ANTICARDIOLIPIN ANTIBODIES, BONE-MARROW TRANSPLANTATION, ANTI-CARDIOLIPIN ANTIBODIES, INTRAVENOUS GAMMA-GLOBULIN, MOLECULAR-WEIGHT HEPARIN, LOW-DENSITY-LIPOPROTEIN, VIVO THROMBOSIS MODEL, X BXSB F1-MICE, FETAL LOSS

Abstract

The antiphospholipid antibody syndrome (APS) is characterized by thrombocytopenia, recurrent thromboembolic phenomena and recurrent fetal loss, in association with anticardiolipin antibodies (aCL) and/or lupus anticoagulant (LA). Owing to the ethical and practical restrictions of experimentation on humans, we have to look to animal experimentation to broaden our knowledge of the pathogenesis and management of APS. Work has been carried out predominantly on strains of naive mice in which APS has been induced, passively and actively, using autoantibodies, autoantigens and other antigens. Studies of autoimmune-prone mice and naive rabbits are present in the literature, to a lesser degree. We review the various animal models of the pathogenesis of APS, whether spontaneous or induced, which have been developed over the years. Although several of the models have provided insights into the relationship between antiphospholipid antibodies and fetal loss, very few give guidance to explain the link with thrombosis. Novel or experimental therapeutic regimens have to be tested on appropriate animal models before any kind of human clinical trials may proceed. The regimens devised thus far are also reviewed.