Immunogenetics of Systemic Lupus Erythematosus in Spanish Patients: Differential HLA Markers

HLA-DR3 antigen included in the compound phenotype B18BfF1 (but not the one linked to the B8BfS compound phenotype) was found to be significantly increased in our SLE patients. It is remarkable that in our Southern-Mediterranean population, B18BfF1DR3 individuals (but not B8BfSDR3) are prone to SLE...

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Bibliographic Details
Published in:Immunobiology (1979) 1991-08, Vol.182 (5), p.465-471
Main Authors: Gémez-Reino, Juan J., Martínez-Laso, Jorge, Vicario, José L., Paz-Artal, Estela, Aragón, Angel, Martín-Villa, José M., Dolores De Juan, M., Pérez-Aciego, Paloma, Arnaiz-Villena, Antonio
Format: Article
Language:English
Subjects:
Autoantibodies
Biological and medical sciences
Histocompatibility Antigens Class I - analysis
Histocompatibility Antigens Class II - analysis
Histocompatibility Testing
HLA Antigens - analysis
HLA-B Antigens - analysis
HLA-C Antigens - analysis
Humans
Kidney Diseases - complications
Kidney Diseases - immunology
Lupus Erythematosus, Systemic - complications
Lupus Erythematosus, Systemic - genetics
Lupus Erythematosus, Systemic - immunology
Medical sciences
Phenotype
Sarcoidosis. Granulomatous diseases of unproved etiology. Connective tissue diseases. Elastic tissue diseases. Vasculitis
Spain
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Summary:HLA-DR3 antigen included in the compound phenotype B18BfF1 (but not the one linked to the B8BfS compound phenotype) was found to be significantly increased in our SLE patients. It is remarkable that in our Southern-Mediterranean population, B18BfF1DR3 individuals (but not B8BfSDR3) are prone to SLE with renal disease, in contrast with other Northern European and Caucasoid populations. Also, patients with autoantibodies to Ro/La have a significant increase of the B8DR3 compound phenotype. Production of autoantibodies against Ro alone was associated to DR2 and production of anti-Sm/nRNP to DR3 (either B18BfF1 or B8BfS associated) only in the subgroup without renal disease. The distinctive HLA and autoimmune associations to SLE with and without renal disease suggests that both clinical forms may not share a common identical pathogenesis.
ISSN:0171-2985
1878-3279
DOI:10.1016/S0171-2985(11)80210-X