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  • 1
    Electronic Resource
    Electronic Resource
    Family studies in scleroderma (systemic sclerosis) demonstrating an HLA-linked increased chromosomal breakage rate in cultured lymphocytes (1988)
    Springer
    Human genetics 〈Berlin〉 81 (1988), S. 64-70 
    Details
    ISSN: 1432-1203
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary An increased chromosomal breakage rate (ICBR) was found in 27 of 28 patients with scleroderma (systemic sclerosis, SS)-5 with the syndrome including calcinosis cutis, Raynaud phenomenon, esophagus hypomotility, sclerodactyly and telangiectasia (CREST), 4 incomplete CREST, 1 overlapping syndrome, 18 progressive systemic sclerosis (PSS). Not only the patients, but also about half of their first-degree relatives showed an increased chromosomal breakage rate (more than 5 breaks per 100 metaphases). This character segregated as a dominant marker in nine families of scleroderma patients. In the six informative of the nine families, the ICBR trait showed close linkage with the HLA region on chromosome 6 (total lod score 5.5 at θ=0). In these families, ICBR was predominantly observed in linkage with HLA haplotype A1, Cw7, B8, C4AQ0B1, DR3 which is frequently observed in autoimmune diseases. The nature of the agent inducing chromosomal breakage in cultured lymphocytes of some, but not all family members of scleroderma patients remains to be clarified.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00283732
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  • 2
    Electronic Resource
    Electronic Resource
    Southern blot analysis of HLA-DP gene polymorphisms in Caucasoid rheumatoid arthritis (RA) patients and controls (1989)
    Springer
    Immunogenetics 30 (1989), S. 149-155 
    Details
    ISSN: 1432-1211
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract Despite extensive analysis of the incidence ofHLA-DR andHLA-DQ allele frequencies in defined autoimmune disease groups, there is very little information available onHLA-DP allele frequencies. This is largely becauseHLA-DP typing has until recently been restricted to primed lymphocyte typing (PLT). However, allelic polymorphism of theHLA-DP subregion can now be studied by Southern blot analysis or genotyping withDPA1 andDPB1 probes. By direct counting of allele-specific DNA fragments, we have analyzed the frequencies of five majorDP genotypes (DPw1, DPw2, DPw3/6, DPw4, andDPw5), in a large number of Caucasoid rheumatoid arthritis (RA) patients (n=74), and controls (n=91). The predicted frequency ofDP alleles in both patient and control groups was comparable to PLT-determinedDP allele frequencies in normal Caucasoids. However, the gene frequency ofDPw4 was increased in the RA patients, with 51% of the patients studied scoring asDPw4, 4 homozygotes. With the exception of one possible combination (DPw5 andDRw6) in the controls, no significant linkage disequilibrium was detected betweenDP andDR alleles in either patient or control groups. Thus the prevalence ofDPw4 in the RA patients is independent of any disease association with theDR loci, and may represent a new class II association with RA.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02421199
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  • 3
    Electronic Resource
    Electronic Resource
    Fetal-maternal HLA compatibility confers susceptibility to systemic sclerosis (1997)
    Springer
    Immunogenetics 47 (1997), S. 17-22 
    Details
    ISSN: 1432-1211
    Keywords: Key words Compatibility ; HLA ; Systemic sclerosis ; Susceptibility ; Fetal-maternal
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract  Systemic sclerosis (SSc) is a disease of unknown origin, which occurs predominantly in women after childbearing years. There are prominent clinical and histopathologic similarities between SSc and chronic graft-versus-host disease (GVHD). GVHD can occur after blood transfusions or after transplantation with HLA-compatible bone marrow. Here we examined the hypothesis that SSc may be caused by fetal cells crossing the placenta into the maternal circulation and providing donor lymphocytes which recognize disparate HLA antigens, resulting in a reaction similar to chronic GVHD. To test the hypothesis we analyzed the inheritance of HLA class I and class II haplotypes in the families of 37 SSc patients and 42 control individuals. Twenty-six (70.2%) SSc patients had HLA class II alleles compatible either for their offspring or mother, compared with only nine (21%) control individuals. The four patients with juvenile onset SSc we analyzed had alleles compatible with their mothers. These results suggest that in some patients, SSc may, indeed, be a form of chronic GVHD caused by fetal or maternal cells which have crossed the placenta during pregnancy and have remained unrecognized by the host due to class II HLA compatibility, and that subsequent activation of these cells by as yet unknown stimuli result in the development of the disease.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s002510050321
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  • 4
    Electronic Resource
    Electronic Resource
    HLA-DQw7 is a disease severity marker in patients with rheumatoid arthritis (1989)
    Springer
    Immunogenetics 30 (1989), S. 119-122 
    Details
    ISSN: 1432-1211
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02421540
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  • 5
    Electronic Resource
    Electronic Resource
    HLA class II restriction of autoantibody production in patients with systematic lupus erythematosus (1991)
    Springer
    Immunogenetics 33 (1991), S. 276-280 
    Details
    ISSN: 1432-1211
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00230506
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  • 6
    Electronic Resource
    Electronic Resource
    HLA-DRB1 amino acid disparity is the major stimulus of interleukin-2 production by alloreactive helper T-lymphocytes (1998)
    Springer
    Immunogenetics 47 (1998), S. 310-317 
    Details
    ISSN: 1432-1211
    Keywords: Key words Alloreactivity ; HLA-DR antigens ; Interleukin-2 ; Helper T lymphocytes ; Histocompatibility
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract  The generation of interleukin-2 (IL-2)-mediated helper activity is a central step in the immune response induced by allogeneic histocompatibility antigens, and IL-2-producing helper T-lymphocyte precursor (HTLp) frequencies have been proposed as a measure of alloreactivity in transplant recipients. We analyzed the influence of HLA-matching on the alloresponse of HTLp in limiting dilution assays derived from healthy individuals. Mean HTLp frequencies were significantly higher in HLA-DR antigen-mismatched than HLA-DR-matched combinations. Significant differences in the effect of one or two mismatched HLA-DR antigens on mean HTLp frequencies were also detected. Mean HLA class I (HLA-A, -B, -Cw) mismatches were not significantly different in each group and had no apparent influence on HTLp frequencies. Analysis of HLA protein sequence disparities revealed no significant difference in the number of mismatched amino acid residues at the HLA-DRB1 locus between one and two HLA-DR antigen-mismatched combinations but correlated strongly with HTLp frequency. The positive correlation was evident with mismatched residues in the beta sheet and alpha helical regions of the HLA-DRB1 molecule, suggesting a predominant influence of bound peptides in the stimulation of alloreactive helper cells. This finding was supported by analysis of the location of individual residue mismatches. Evidence of an effect of polymorphism in the CD4-binding region in the β-2 domain of HLA-DRB1 molecules was also found. Our results demonstrate the major influence of HLA-DR amino acid sequence mismatching on alloreactive HTLp frequencies but also suggest that additional genetic or environmental influences affect the alloreactive helper T-cell repertoire.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s002510050363
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