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Research Article Free access | 10.1172/JCI115704

Association of polar amino acids at position 26 of the HLA-DQB1 first domain with the anticentromere autoantibody response in systemic sclerosis (scleroderma).

J D Reveille, D Owerbach, R Goldstein, R Moreda, R A Isern, and F C Arnett

Department of Internal Medicine, University of Texas Medical School, Houston 77225.

Find articles by Reveille, J. in: JCI | PubMed | Google Scholar

Department of Internal Medicine, University of Texas Medical School, Houston 77225.

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Department of Internal Medicine, University of Texas Medical School, Houston 77225.

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Department of Internal Medicine, University of Texas Medical School, Houston 77225.

Find articles by Moreda, R. in: JCI | PubMed | Google Scholar

Department of Internal Medicine, University of Texas Medical School, Houston 77225.

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Department of Internal Medicine, University of Texas Medical School, Houston 77225.

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Published April 1, 1992 - More info

Published in Volume 89, Issue 4 on April 1, 1992
J Clin Invest. 1992;89(4):1208–1213. https://doi.org/10.1172/JCI115704.
© 1992 The American Society for Clinical Investigation
Published April 1, 1992 - Version history
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Abstract

HLA class II alleles (detected by DNA typing) were determined in 116 Caucasians with systemic sclerosis positive and negative for anticentromere autoantibodies (ACA). Significantly increased frequencies of HLA-DR5(DRw11) (P = 0.009) and the Dw13(DRB1*0403, *0407) subtypes of DR4 (probability corrected, Pc = 0.005) were seen in ACA positive patients, and HLA-DR1 and DRw8 were also increased. These findings appeared to reflect linkage disequilibrium of DR5(DRw11) and many DR4(Dw13) haplotypes with HLA-DQw7 and DR1 with DQw5. In fact, the presence of a DQB1 allele having a polar glycine or tyrosine at position 26 of the DQB1 first domain versus a hydrophobic leucine accounted for 100% of ACA positive Caucasian systemic sclerosis patients compared to 69% of the ACA negative SS patients (P = 0.0008) and 71% of Caucasian controls (P = 0.0003) as well as all 7 ACA patients of non-Caucasian background. Furthermore, the genotype frequency of DQB1 alleles lacking leucine at position 26 was 73% in ACA positive SS patients, compared to 42% of ACA negative patients (P = 1.2 x 10(-5)) and 38% of controls (P = 5.8 x 10(-7)). These data, then, suggest that the second hypervariable region of the HLA-DQB1 chain may form the candidate epitope associated with the ACA response.

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