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Characterization of the murine autoimmune disease resembling human lupus induced by antibodies to non‐bilayer phospholipid arrangements
Author(s) -
Baeza Carlos Wong,
España Luis,
Ramírez Carlos Wong,
Pando Rogelio Hernández,
Baeza Isabel
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.2_supplement.471
Subject(s) - autoimmune disease , systemic lupus erythematosus , immunology , antibody , immune system , monoclonal antibody , autoimmunity , medicine , chemistry , pathology , disease
Antibodies against a phospholipid arrangement different to the lipid bilayer called non‐bilayer phospholipid arrangement (NPA) induced an autoimmune‐like murine disease, which exhibited features similar to human lupus. The autoimmune‐like murine disease was induced by injecting BALB/c or NIH mice either with a monoclonal antibody specific to NPA, or with sera from mice which already had developed the autoimmune disease, or with liposomes treated with the NPA inductors chlorpromazine or procainamide, or with these NPA inductors alone. All these procedures revealed the involvement of antibodies to NPA in induced this autoimmune‐like disease. Mice developed in some skin areas alopecia, particularly on the face, which were more extensive in NIH than in BALB/c mice. Histopathology showed abnormalities only in skin and kidney, immunofluorescence showed linear deposition of immune complexes along dermal‐epidermal junction, like in the human, and along the basement membranes of glomerular capillaries and in the mesangial matrix. Knockout IL‐4 BALB/c mice only developed a light autoimmune disease compared with the wild mice, which revealed the important role of this cytokine in this autoimmune disease. This experimental model of lupus might contribute to a better understanding of the molecular and immunological basis of autoimmune diseases like lupus and probably toward the development of better human therapeutic strategies.