Abstract
The clinical associations of antiphospholipid antibodies (aPL) are well recognized but the mechanism(s) causing the production of these antibodies are not yet known. We demonstrated the induction of pathogenic aPL antibodies that caused intrauterine fetal death and transverse myelopathy due to spinal cord infarction in mice by immunization with foreign beta2GPI. We also induced aPL and anti-beta2-GPI in mice by immunization with PL-binding viral peptides and hypothesized that in APS patients, aPL may be induced by beta2GPI-like-PL-binding products of common human bacteria and viruses.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
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Review
MeSH terms
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Animals
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Antibodies, Antiphospholipid / biosynthesis
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Antibodies, Antiphospholipid / immunology*
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Antibodies, Monoclonal / immunology
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Antibody Specificity
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Antigens, Bacterial / immunology
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Antigens, Viral / immunology
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Antiphospholipid Syndrome / etiology*
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Antiphospholipid Syndrome / immunology
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Autoantigens / chemistry
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Autoantigens / immunology*
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Autoimmune Diseases / etiology*
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Autoimmune Diseases / immunology
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Cross Reactions
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Disease Models, Animal
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Female
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Fetal Death / etiology*
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Fetal Death / immunology
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Glycoproteins / chemistry
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Glycoproteins / immunology*
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Humans
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Immunization
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Infarction / etiology
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Infarction / immunology
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Mice
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Molecular Mimicry
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Myelitis, Transverse / etiology*
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Myelitis, Transverse / immunology
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Peptide Fragments / immunology*
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Pregnancy
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Rabbits
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Spinal Cord / blood supply
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Thrombophilia / etiology
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Thrombophilia / immunology
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beta 2-Glycoprotein I
Substances
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Antibodies, Antiphospholipid
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Antibodies, Monoclonal
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Antigens, Bacterial
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Antigens, Viral
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Autoantigens
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Glycoproteins
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Peptide Fragments
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beta 2-Glycoprotein I