
Independent association of HLA-DPB1*02:01 with rheumatoid arthritis in Japanese populations
Author(s) -
Hiroshi Furukawa,
Shomi Oka,
Kota Shimada,
Atsushi Hashimoto,
Akiko Komiya,
Shinichiro Tsunoda,
Arnold J. Suda,
Satoshi Ito,
Koichiro Saisho,
Masao Kameyama,
Satoshi Shinohara,
Takeo Sato,
Katsuya Nagatani,
Seiji Minota,
Toshihiro Matsui,
Naoshi Fukui,
Shoji Suzuki,
Hajime Sano,
Kiyoshi Migita,
Shinya Nagaoka,
Shigeto Tohma
Publication year - 2018
Publication title -
plos one
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.99
H-Index - 332
ISSN - 1932-6203
DOI - 10.1371/journal.pone.0204459
Subject(s) - rheumatoid arthritis , odds ratio , medicine , immunology , genetic predisposition , etiology , allele , confidence interval , autoimmune disease , disease , antibody , genetics , biology , gene
Objective Rheumatoid arthritis (RA) is a chronic autoimmune disease characterized with joint destructions; environmental and genetic factors were thought to be involved in the etiology of RA. The production of anti-citrullinated peptide antibodies (ACPA) is specifically associated with RA. DRB1 is associated with the susceptibility of RA, especially ACPA-positive RA [ACPA(+)RA]. However, a few studies reported on the independent associations of DPB1 alleles with RA susceptibility. Thus, we investigated the independent association of DPB1 alleles with RA in Japanese populations. Methods Association analyses of DPB1 were conducted by logistic regression analysis in 1667 RA patients and 413 controls. Results In unconditioned analysis, DPB1*04 : 02 was nominally associated with the susceptibility of ACPA(+)RA ( P = 0.0021, corrected P ( Pc ) = 0.0275, odds ratio [OR] 1.52, 95% confidence interval [CI] 1.16–1.99). A significant association of DPB1*02 : 01 with the susceptibility of ACPA(+)RA was observed, when conditioned on DRB1 ( P adjusted = 0.0003, P c adjusted = 0.0040, OR adjusted 1.47, 95%CI 1.19–1.81). DPB1*05 : 01 was tended to be associated with the protection against ACPA(+)RA, when conditioned on DRB1 ( P adjusted = 0.0091, P c adjusted = 0.1184, OR adjusted 0.78, 95%CI 0.65–0.94). When conditioned on DRB1 , the association of DPB1*04 : 02 with ACPA(+)RA was disappeared. No association of DPB1 alleles with ACPA-negative RA was detected. Conclusion The independent association of DPB1*02 : 01 with Japanese ACPA(+)RA was identified.