Open AccessNo support for HLA–DQ encoded susceptibility in rheumatoid arthritis
Author(s) -
De Vries Niek,
Van Elderen Claudia,
Tijssen Henk,
Van Riel Piet L. C. M.,
>Van De Putte Leo B. A.
Publication year - 1999
Publication title -
arthritis & rheumatism
Language(s) - English
Resource type - Journals
eISSN - 1529-0131
pISSN - 0004-3591
DOI - 10.1002/1529-0131(199908)42:8<1621::aid-anr9>3.0.co;2-0
Subject(s) - rheumatoid arthritis , hla dq , medicine , human leukocyte antigen , immunology , computational biology , genetics , biology , antigen , gene , allele , haplotype
Objective To test predictions based on data from immunogenetic and peptide‐binding studies of collagen‐induced arthritis in mice, in which it has been suggested that susceptibility to rheumatoid arthritis (RA) might be determined by the interaction between susceptibility alleles at the HLA–DQ locus and protective alleles at the HLA–DRB1 locus (including susceptibility effects for HLA–DQ7 and DQ8). Methods Predictions based on these models were tested in 166 healthy controls and 167 patients with RA, all of whom were typed for HLA–DRB1 and HLA–DQ alleles. Results In this population, HLA–DQ7 did not encode an increased risk for RA. This lack of susceptibility effect of HLA–DQ7 could not be attributed to competing HLA–DQ susceptibility alleles, protective HLA–DRB1 alleles, or the absence of DQA1*0301. Conclusion These observations do not support the DR/DQ hypothesis in its present form.