Rheumatology, Vol 38, 591-601, Copyright © 1999 by British Society for Rheumatology
EL Radway-Bright, M Inanc and DA Isenberg
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.
REVIEWS
Animal models of the antiphospholipid syndrome
Bloomsbury Rheumatology Unit, Department of Medicine, University College London, UK.
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