Antibodies to non‐bilayer phospholipid arrangements induce a murine autoimmune disease resembling human lupus

Antibodies recognizing non‐bilayer phospholipid arrangements (NPA) in membrane models and in cell membranes in vivo, triggered an autoimmune‐like disease in mice. This exhibited features similar to human lupus and was induced by injecting mice either with the H308 monoclonal antibody specific to NPA...

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Bibliographic Details
Published in:European journal of immunology 2004-02, Vol.34 (2), p.576-586
Main Authors: Baeza, Isabel, Leyva, Emma, Campos, Begoña, Lara, Mónica, Ibáñez, Miguel, Farfán, Norberto, Orozco, Héctor, Flores‐Romo, Leopoldo, Hernández‐Pando, Rogelio, Wong, Carlos
Format: Article
Language:English
Subjects:
Animals
Anti-Arrhythmia Agents - adverse effects
Anti-Arrhythmia Agents - immunology
Antipsychotic Agents - adverse effects
Antipsychotic Agents - immunology
Autoantibodies
Autoantibodies - immunology
Autoimmune diseases
Autoimmune Diseases - immunology
Autoimmune Diseases - pathology
Chlorpromazine - adverse effects
Chlorpromazine - immunology
Disease Models, Animal
Female
Liposomes - immunology
Lupus‐like
Magnetic Resonance Spectroscopy
Male
Mice
Mice, Inbred BALB C
Murine‐lupus
Non‐bilayer phospholipids
Phospholipids - immunology
Procainamide - adverse effects
Procainamide - immunology
Specific Pathogen-Free Organisms
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Summary:Antibodies recognizing non‐bilayer phospholipid arrangements (NPA) in membrane models and in cell membranes in vivo, triggered an autoimmune‐like disease in mice. This exhibited features similar to human lupus and was induced by injecting mice either with the H308 monoclonal antibody specific to NPA, with sera from mice which already had developed the autoimmune disease, or withliposomes treated with the NPA inductors chlorpromazine or procainamide; or with these NPA inductors alone. All these procedures revealed the involvement of antibodies to non‐bilayer phospholipids in inducing this autoimmune‐like disease. Unraveling the mechanisms of these antibodies might contribute to a better understanding of the molecular and immunological basis of autoimmune diseases like lupus and, hopefully, towards the development of better therapeutic strategies.
ISSN:0014-2980
1521-4141
DOI:10.1002/eji.200324177