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  • 1
    Electronic Resource
    Electronic Resource
    Immunoglobulin allotypes are not associated with HLA-antigens, autoantibodies and clinical symptoms in systemic lupus erythematosus (1991)
    Springer
    Rheumatology international 11 (1991), S. 179-182 
    Details
    ISSN: 1437-160X
    Keywords: Immunoglobulin allotypes ; Systemic lupus erythematosus ; Genetics ; Gm ; Km ; HLA-antigens ; Autoantibodies ; Clinical symptoms
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Immunoglobulin heavy chain (G1m, G2m, G3m, A2m) and kappa light chain (Km) allotype and phenotype frequencies of 323 central European Caucasian patients with systemic lupus erythematosus (SLE) were examined and correlated with various genetic, serologic and clinical markers of SLE. No significant associations were found between immunoglobulin allotypes or phenotypes and all 20 parameters tested (nephritis, vasculitis, arthralgias, photosensitivity, discoid lesions, central nervous system disease, Raynaud's phenomenon, sex, anti-Ro, anti-La, anti-nRNP, HLA-DR1-DR7, HLA phenotypes B8-DR3, B7-DR2). It could therefore be assumed that Gm, A2m and Km allotypes were not associated with HLA-antigens and had no influence on the serologic and clinical expression of SLE.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00332558
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  • 2
    Electronic Resource
    Electronic Resource
    HLA class II genes and antibodies against recombinant U1-nRNP proteins in patients with systemic lupus erythematosus (1994)
    Springer
    Rheumatology international 14 (1994), S. 63-69 
    Details
    ISSN: 1437-160X
    Keywords: Systemic lupus erythematosus ; Recombinant U1-nRNP proteins ; Genetics
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract To investigate a possible involvement of HLA-class II alleles in the genetic predisposition for the formation of anti-U1-nRNP antibody in systemic lupus erythematosus (SLE), genomic DNA of 178 patients was typed for the DRB1, DQA1 and DQB1 alleles using a polymerase chain reaction (PCR) and non-radioactive-oligonucleotide typing. Antibodies against recombinant U1-nRNP proteins (U1-A- U1-C-and 70K-protein) were determined by ELISA. Anti-U1-C antibody was found in 26 (14.7%), anti-U1-A in 34 (19.2%) and anti-70K in 17 (9.6%) patients. A joint occurrence was observed for these antibodies against the recombinant U1-nRNP proteins: anti-U1-C and anti-U1-A antibodies occurred together more frequently than alone and than together with anti-U1-70K antibodies. The frequency of DRB1 * 04 was slightly increased in the patients with anti-U1-C as compared to the patients without anti-U1-C (P〈0.05, Pcorr=n.s., RR=2.4). The DQA1 * 0301 allele, which is in linkage disequilibrium with DRB1 * 04, is found more frequently in anti-U1-C-positive than in antibody-negative patients. The DQB1 * 0303 allele, detected in 12 of 176 SLE patients, was absent in the patients with any of the antibodies against the U1-nRNP proteins. All these deviations may be due to chance alone. We concluded that the presence of antibodies against recombinant U1-nRNP proteins was not significantly associated with any HLA DRB1, DQA1 and DQB1 allele in our group of SLE patients.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00300249
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  • 3
    Electronic Resource
    Electronic Resource
    Evidence for direct anti-heparin-sulphate reactivity in sera of SLE patients (1994)
    Springer
    Rheumatology international 14 (1994), S. 169-174 
    Details
    ISSN: 1437-160X
    Keywords: Systemic lupus erythematosus ; Lupus nephritis ; Heparan sulphate ; Antibodies
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Recently it has been suggested that anti-dsDNA antibodies (Abs) promote tissue damage in systemic lupus erythematosus (SLE) by cross-reactivity with highly negatively charged tissue components such as heparan sulphate (HS), the major glycosaminoglycan of the glomerular basement membrane (GBM). Other authors, however, support the theory of DNA-anti-dsDNA immune complex deposition in situ. To further elucidate the possible role of HS antibodies, we developed a new ELISA system with heparan sulphate bound to solid phase. SLE patients (n=40) showed a higher reactivity against HS (mean=28.4, SD=34.3) as compared to normal donors (n=28, mean=15.2, SD=6.3) and patients with rheumatoid arthritis (n=35, mean=14.3, SD=6.4). The addition of native dsDNA or HS to SLE sera was followed by a dose-dependent reduction in anti-HS reactivity. In contrast, in an anti-dsDNA ELISA, no reduction was observed when HS was added to SLE sera. An increase in reactivity was observed when SLE sera with and without a prior incubation with dsDNA were digested with DNAse I or II. After the purification of serum samples by protein A sepharose under dissociative conditions, seven out of eight SLE patients showed an increase in anti-HS reactivity. No correlation of the anti-HS Abs was found with organ involvement or other serological parameters. We concluded, that there is evidence for a direct anti-HS Ab reactivity in SLE sera. A part of these antibodies seems to show low avidity anti-dsDNA cross-reactivity.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00579703
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    Paper (German National Licenses)
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