HLA A24 and SLE

[Mike Bartolatz]

Titre du document / Document title
Soluble HLA-I (s-HLA-I) synthesis in systemic lupus erythematosus
Auteur(s) / Author(s)
ADAMASHVILI Irena (1) ; WOLF Robert (2) ; AULTMAN Donnie (1) ; MILFORD Edgar L. (3) ; JAFFE Stephen (4) ; HALL Vicky (2) ; PRESSLY Thomas (2) ; MINAGAR Alireza (4) ; KELLEY Roger (4) ;
Affiliation(s) du ou des auteurs / Author(s) Affiliation(s)
(1) Department of Surgery, Louisiana State University Health Sciences Center, P.0. Box 33932, Shreveport, LA 71130-3932, ETATS-UNIS
(2) Department of Rheumatology, Louisiana State University Health Sciences Center, Shreveport, Louisiana, ETATS-UNIS
(3) Renal Transplantation and Tissue Typing Laboratory, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, ETATS-UNIS
(4) Department of Neurology, Louisiana State University Health Sciences Center, Shreveport, Louisiana, ETATS-UNIS

Résumé / Abstract
Our objective was to study a possible contribution of major histocompatibility complex (MHC) genes to soluble HLA-I synthesis in patients with systemic lupus erythematosus (SLE). Solid-phase enzyme-linked immunoassay (ELISA) was used to measure sHLA-I in the sera of 20 patients with SLE and 76 normal controls with known HLA phenotypes. Serial serum samples (n=108) from the above group of patients (n=19) were further investigated by sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS-PAGE) and immunoblotting. Soluble HLA-I levels were abnormally higher in patients with SLE than normal controls (P<0.0002). No complete HLA haplotype has been identified to be correlated with high or low sHLA-I secretion. Only the sera of HLA-A23- or -A24- (splits of HLA-A9) positive individuals were found to contain high sHLA-I concentrations in both populations studied. The difference between sHLA-I of HLA-A24 patients (n=7) and HLA-A24 normal controls (n=19) was statistically highly significant (P<0.0079). The results suggest that HLA-A24 may confer additional risk of more severe disease expression in female patients with SLE. The data imply that SLE patients carrying 39-kDa sHLA-I have increased risk of developing renal disease. A higher prevalence of 35-37 kDa was observed in patients with mild disease. Interestingly, 44-46 kDa was the predominant molecular form of sHLA-I in SLE patients with lymphocytosis with no evidence of organ involvement. Notably, all these variations were not reflected by differences in HLA phenotypes, with the exception of HLA-A24-positive patients, in whom the 44-46-kDa form occurs consistently but not exclusively. In summary, the results show a genetic heterogeneity of SLE with MHC control of the expression of sHLA-I concentrations and possible involvement of disease-associated factors that might potentiate a specific sHLA-I molecule synthesis.
Revue / Journal Title
Rheumatology international (Rheumatol. int.) ISSN 0172-8172
Source / Source
2003, vol. 23, no6, pp. 294-300 [7 page(s) (article)] (42 ref.)
Langue / Language
Anglais

Editeur / Publisher
Springer, Berlin, ALLEMAGNE (1981) (Revue)

Mots-clés anglais / English Keywords
Molecular biology ; Immunopathology ; Autoimmune disease ; Systemic disease ; Connective tissue disease ; Skin disease ; Soluble form ; HLA-System ; ELISA assay ; Pathogenesis ; Human ; Systemic ; Lupus erythematosus ;
Mots-clés français / French Keywords
Biologie moléculaire ; Immunopathologie ; Maladie autoimmune ; Maladie système ; Tissu conjonctif pathologie ; Peau pathologie ; Forme soluble ; Système HLA ; Technique ELISA ; Pathogénie ; Homme ; Systémique ; Lupus érythémateux ;

002b06a ;
Mots-clés espagnols / Spanish Keywords
Biología molecular ; Inmunopatología ; Enfermedad autoinmune ; Enfermedad sistémica ; Tejido conjuntivo patología ; Piel patología ; Forma soluble ; Sistema HLA ; Técnica ELISA ; Patogenia ; Hombre ; Sistémico ; Lupus eritematoso ;
Mots-clés d'auteur / Author Keywords
Enzyme-linked immunosorbent assay ; Major histocompatibility complex ; Soluble human leukocyte antigens ; Systemic lupus erythematosus ;
Localisation / Location
INIST-CNRS, Cote INIST : 18212, 35400011607489.0050


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Nº notice refdoc (ud4) : 15328708