We also identified an association with ACPA(+) RA at HLA-A position 77 (p = 2.7 × 10(-8), OR = 0.85) in 7,279 ACPA(+) RA case and 15,870 control subjects.
HLA-A, HLA-DRB1, and 8 additional markers showed evidence of linkage in the presence of association with RA (using the extended transmission disequilibrium test [ETDT]).
Our results suggested the possibility that the susceptibility to RA is controlled by the interaction of HLA-A and DRBl genes or by that of HLA-A and DPBl genes in different patient subgroups.
One of the extended haplotypes reported in a number of studies for FS and rheumatoid arthritis (summarized as HLA-A*02;Cw*0501; B*44;TNFb5;TNFa6;TNFd4;C4A*3;C4BQ*0;DRB1*0 401;DQB1*0301) is likely to be attributable to strong primary association with HLA-DRB1*0401, rather than to epistatic interaction between these loci.
Eighty-five Arab patients in Kuwait with classical and definite rheumatoid arthritis were typed to examine the frequency of HLA-A, B, C, and DR antigens.
The frequency of HLA-A, -B, and -DR alloantigens was studied in 46 patients with primary Sjögren's syndrome (pSS), 14 patients with secondary Sjögren's syndrome (sSS) and rheumatoid arthritis (RA), 26 classical RA patients without clinical or histologic evidence of Sjögren's syndrome (SS) and 172 normal controls.
We have studied HLA-A, B, C, and DR antigens in 75 unrelated white families, each with multiple cases of adult-onset definite or classical rheumatoid arthritis (RA) (by ARA criteria).
In an attempt to study the variation of associations between HLA and rheumatoid disease a population of 44 Ashkenazi and 29 non-Ashkenazi patients with Rheumatoid Arthritis were tested for HLA-A, B, C and DR antigens and compared with the relevant control groups.
Patients with Sjögren's syndrome (SS) in association with either Rheumatoid Arthritis (RA), Systemic Lupus Erythematosus (SLE) or Sclerodactyly were tested for HLA-A, B and Dr antigens and the phenotypes of the 4th component of complement (CA).
One hundred and eighteen unrelated Greek patients with classic rheumatoid arthritis (RA) were tissue-typed for HLA-A, -B, -DR antigens and the frequency was compared to that of healthy controls.
HLA-A, B, C and D typing was performed in 19 patients with primary Sjögren's syndrome (primary SS) and in 15 patients with rheumatoid arthritis (RA) and secondary Sjögren's syndrome (RA-SS).