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Research Article Free access | 10.1172/JCI115927
Division of Rheumatic Diseases, Hospital for Special Surgery-Cornell University Medical Center, New York 10021.
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Division of Rheumatic Diseases, Hospital for Special Surgery-Cornell University Medical Center, New York 10021.
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Division of Rheumatic Diseases, Hospital for Special Surgery-Cornell University Medical Center, New York 10021.
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Division of Rheumatic Diseases, Hospital for Special Surgery-Cornell University Medical Center, New York 10021.
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Published September 1, 1992 - More info
A subset of patients with systemic lupus erythematosus has autoantibodies to acidic phospholipids. Since lipids are poor immunogens, the mechanism responsible for the induction of these antibodies is unclear. Immunization of a normal rabbit and normal mice with purified human beta 2-glycoprotein I (apolipoprotein H) resulted in the production of high levels of two non-cross-reactive antibody populations, anti-apolipoprotein H, and antiphospholipid. The antiphospholipid antibodies had binding specificities indistinguishable from autoantibodies obtained from human and murine lupus. These findings suggest a novel mechanism for the induction of antiphospholipid autoantibodies.
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