Nomenclature for Factors of the HLA System, 1987

Bodmer, Walter F.; Albert, E. D.; Bodmer, JG; Dupont, Bo; Mach, Bernard; Mayr, Wolfgang R.; Sasazuki, Takehiko; Schreuder, G. M. T.; Svejgaard, A.; Terasaki, Paul I.

doi:10.1007/978-1-4612-3552-1_14

Cited by 76 publications

(46 citation statements)

References 26 publications

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“…HLA-DQw3 comprises HLA-DQB 1*0301 (DQw7) (linked to HLA-DR5 (DRwl 1) as well as other DR specificities), DQw8 (associated with HLA-DR4), and DQw9 (associated with HLA-DR9 and occasionally HLA-DR7) (56). The HLA-DQB 1 alleles comprising HLA-DQw3 share striking sequence homology (Table VI).…”

Section: Discussionmentioning

confidence: 99%

Association of amino acid sequences in the HLA-DQB1 first domain with antitopoisomerase I autoantibody response in scleroderma (progressive systemic sclerosis).

Reveille¹,

Durban²,

Clair³

et al. 1992

J. Clin. Invest.

132

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Previous studies in Caucasians with progressive systemic sclerosis (PSS) have suggested associations of antitopoisomerase I (antitopo I) autoantibodies with either serologically defined HLA-DR2 or DR5. To better define class II HLA associations with the antitopo I response, 161 PSS patients (132 Caucasians and 29 American blacks) were studied for antitopo I autoantibodies by immunodiffusion and immunoblotting, and their HLA-DRB1, DRB3, DQA1, and DQB1 alleles were determined by restriction fragment length polymorphic analysis and DNA oligotyping. Among Caucasians with antitopo I, HLA-DR5(DRB1*1101-*1104), DRB3*0202 and DQw3 (DQw7,8,9) were significantly increased in frequency. In American blacks, however, only HLA-DQB1 *0301 (DQw7) was significantly increased. The presence of HLA-DQB1 *0301 (DQw7) and other HLA-DQB1 alleles bearing the uncharged polar amino acid residue tyrosine at position 30 of the outermost domain was found in all antitopo I-positive Caucasian PSS patients compared with 66% of antitopo I-negative PSS patients (pc = 0.007) and 70% of normal controls (pc = 0.008), as well as all antitopo I-positive black patients. The association with HLA-DQB1 was independent of HLA-DR5(DRB1*1101-*1 104) or any other HLA-DRB1, DRB3, or DQA1 alleles. Alternative or additional candidate epitopes for this autoimmune response include alanine at position 38 and threonine at position 77 of these same DQB1 alleles. These data suggest that genetic predisposition to the antitopo I response in PSS is associated most closely with the HLA-DQB1 locus. (J. Clin. Invest. 1992. 90:973-980.)

show abstract

Section: Discussionmentioning

confidence: 99%

Association of amino acid sequences in the HLA-DQB1 first domain with antitopoisomerase I autoantibody response in scleroderma (progressive systemic sclerosis).

Reveille¹,

Durban²,

Clair³

et al. 1992

J. Clin. Invest.

132

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“…The different patterns of peptide binding by these two class I molecules are apparently not due to differences in their capacities to bind and present the antigenic peptides, since in both systems the antigenic peptides were used at equal molar concentrations (0.2 MtM). The observed differences in peptide competition between HLA-B37 and HLA-A2.1 most likely represent real differences in the specificity of their peptide binding sites (9,10 (24), it may suggest that these two loci have evolved to provide different peptide-binding specificities. The existence of A-ness and B-ness in the nucleotide sequences of HLA-A and -B genes (25) is also indicative of a functional diversification of these loci.…”

Section: Discussionmentioning

confidence: 99%

HLA-B37 and HLA-A2.1 molecules bind largely nonoverlapping sets of peptides.

Carreño

Anderson²,

Coligan³

et al. 1990

Proc. Natl. Acad. Sci. U.S.A.

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“…PCR products were analyzed for efficiency and specificity of the reaction by electrophoresis and adjusted to comparable concentrations. Subsequently, the amplified fragments were blotted and hybridized to allele specific oligonucleotides as described (13,14 (15). Sequence analysis of the HLA-DRBI locus.…”

Section: Methodsmentioning

confidence: 99%

Homozygosity for the HLA-DRB1 allele selects for extraarticular manifestations in rheumatoid arthritis.

Weyand¹,

Xie²,

Goronzy³

1992

J. Clin. Invest.

209

123

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Seropositive rheumatoid arthritis is genetically linked to a group of HLA-DRB1 alleles sharing a sequence motif within the third hypervariable region. Controversy exists over the role of the distinct allelic variants in affecting not only the risk to develop disease, but also in modifying the expression of the disease. We have stratified 81 patients according to their patterns of disease manifestations and identified the HLA-DRB1 alleles by polymerase chain reaction amplification and subsequent oligonucleotide hybridization. To identify precisely the allelic combinations at the HLA-DRB1 locus, homozygosity was confirmed by locus-specific cDNA amplification and subsequent sequencing. Our study demonstrated a high correlation of allelic combinations of disease-associated HLA-DRB1 alleles with the clinical manifestations. Characteristic genotypes were identified for patients who had progressed toward nodular disease and patients who had developed major organ involvement. Rheumatoid nodules were highly associated with a

show abstract

Nomenclature for Factors of the HLA System, 1987

Cited by 76 publications

References 26 publications

Association of amino acid sequences in the HLA-DQB1 first domain with antitopoisomerase I autoantibody response in scleroderma (progressive systemic sclerosis).

Association of amino acid sequences in the HLA-DQB1 first domain with antitopoisomerase I autoantibody response in scleroderma (progressive systemic sclerosis).

HLA-B37 and HLA-A2.1 molecules bind largely nonoverlapping sets of peptides.

Homozygosity for the HLA-DRB1 allele selects for extraarticular manifestations in rheumatoid arthritis.

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