A twin study of rheumatoid arthritis in the Japanese population

Modern Rheumatology

Volumn 26, Issue 5, 2016, Pages 685-689

  Terao, Chikashi ^a,b,c,d   Ikari, Katsunori ^e   Nakayamada, Shingo ^f   Takahashi, Yusuke ^g   Yamada, Ryo ^a   Ohmura, Koichiro ^a   Hashimoto, Motomu ^a   Furu, Moritoshi ^a   Ito, Hiromu ^a   Fujii, Takao ^a   Yoshida, Shinji ^e   Saito, Kazuyoshi ^f   Taniguchi, Atsuo ^e   Momohara, Shigeki ^e   Yamanaka, Hisashi ^b   Mimori, Tsuneyo ^a   Matsuda, Fumihiko ^a  

^a KYOTO UNIVERSITY GRADUATE SCHOOL OF MEDICINE   (Japan)

^b KYOTO UNIVERSITY   (Japan)

^c BRIGHAM AND WOMEN S HOSPITAL   (United States)

^d BROAD INSTITUTE OF MIT AND HARVARD   (United States)

^e TOKYO WOMEN'S MEDICAL UNIVERSITY   (Japan)

^f UNIVERSITY OF OCCUPATIONAL AND ENVIRONMENTAL HEALTH   (Japan)

^g KYOTO UNIVERSITY   (Japan)

Author keywords

Epidemiological study; Genetics and heritability; Rheumatoid arthritis

Indexed keywords

ADULT; ARTICLE; CONTROLLED STUDY; DISEASE SURVEILLANCE; DIZYGOTIC TWINS; FEMALE; FINLAND; GENETIC PREDISPOSITION; HERITABILITY; HUMAN; JAPANESE (PEOPLE); MAJOR CLINICAL STUDY; MALE; MONOZYGOTIC TWINS; PRIORITY JOURNAL; QUALITY CONTROL; RHEUMATOID ARTHRITIS; SIBLING; UNITED KINGDOM; ARTHRITIS, RHEUMATOID; GENETICS; JAPAN; PREVALENCE; TWINS;

ARTHRITIS, RHEUMATOID; DISEASES IN TWINS; FEMALE; GENETIC PREDISPOSITION TO DISEASE; HUMANS; JAPAN; MALE; PREVALENCE;

EID: 84958522995     PISSN: 14397595     EISSN: 14397609     Source Type: Journal    
DOI: 10.3109/14397595.2015.1135856     Document Type: Article

References (22)

1. C.Terao Genetic contribution to susceptibility and disease phenotype in rheumatoid arthritis. Inflamm Regener. 2014;34(2):71–7.
2. Y.Okada, D.Wu, G.Trynka, T.Raj, C.Terao, K.Ikari, et al. Genetics of rheumatoid arthritis contributes to biology and drug discovery. Nature. 2013;506(7488):376–81.
3. C.Terao, K.Ohmura, M.Katayama, M.Takahashi, M.Kokubo, G.Diop, et al. Myelin basic protein as a novel genetic risk factor in rheumatoid arthritis – a genome-wide study combined with immunological analyses. PLoS One. 2011;6(6):e20457.
4. Y.Okada, C.Terao, K.Ikari, Y.Kochi, K.Ohmura, A.Suzuki, et al. Meta-analysis identifies nine new loci associated with rheumatoid arthritis in the Japanese population. Nat Genet. 2012;44(5):511–16.
5. C.Terao, R.Yamada, K.Ohmura, M.Takahashi, T.Kawaguchi, Y.Kochi, et al. The human AIRE gene at chromosome 21q22 is a genetic determinant for the predisposition to rheumatoid arthritis in Japanese population. Hum Mol Genet. 2011;20(13):2680–5.
6. A.J.MacGregor, H.Snieder, A.S.Rigby, M.Koskenvuo, J.Kaprio, K.Aho, et al. Characterizing the quantitative genetic contribution to rheumatoid arthritis using data from twins. Arthritis Rheum. 2000;43(1):30–7.
7. D.van der Woude, J.J.Houwing-Duistermaat, R.E.Toes, T.W.Huizinga, W.Thomson, J.Worthington, et al. Quantitative heritability of anti-citrullinated protein antibody-positive and anti-citrullinated protein antibody-negative rheumatoid arthritis. Arthritis Rheum. 2009;60(4):916–23.
8. C.M.Deighton, D.J.Walker, I.D.Griffiths, D.F.Roberts The contribution of HLA to rheumatoid arthritis. Clin Genet. 1989;36(3):178–82.
9. E.A.Stahl, D.Wegmann, G.Trynka, J.Gutierrez-Achury, R.Do, B.F.Voight, et al. Bayesian inference analyses of the polygenic architecture of rheumatoid arthritis. Nat Genet. 2012;44(5):483–9.
10. A.J.Svendsen, K.O.Kyvik, G.Houen, P.Junker, K.Christensen, L.Christiansen, et al. On the origin of rheumatoid arthritis:the impact of environment and genes – a population based twin study. PLoS One. 2013;8(2):e57304.
11. H.A.HajHensvold A, P.K.Magnusson, V.Joshua, M.Hansson, L.Israelsson, R.Ferreira, et al. Environmental and genetic factors in the development of anticitrullinated protein antibodies (ACPAs) and ACPA-positive rheumatoid arthritis:an epidemiological investigation in twins. Ann Rheum Dis. 2013;17:44.
12. H.Yamanaka, S.Tohma Potential impact of observational cohort studies in Japan on rheumatoid arthritis research and practice. Mod Rheumatol. 2006;16(2):75–6.
13. C.Terao, M.Hashimoto, K.Yamamoto, K.Murakami, K.Ohmura, R.Nakashima, et al. Three groups in the 28 joints for rheumatoid arthritis synovitis – analysis using more than 17,000 assessments in the KURAMA database. PLoS One. 2013;8(3):e59341.
14. D.Aletaha, T.Neogi, A.J.Silman, J.Funovits, D.T.Felson, C.O.BinghamIII, et al. 2010 Rheumatoid arthritis classification criteria:an American College of Rheumatology/European League Against Rheumatism collaborative initiative. Arthritis Rheum. 2010;62(9):2569–81.
15. P.K.Gregersen, J.Silver, R.J.Winchester The shared epitope hypothesis. An approach to understanding the molecular genetics of susceptibility to rheumatoid arthritis. Arthritis Rheum. 1987;30(11):1205–13.
16. C.Terao, K.Ikari, K.Ohmura, T.Suzuki, T.Iwamoto, K.Takasugi, et al. Quantitative effect of HLA-DRB1 alleles to ACPA levels in Japanese rheumatoid arthritis:no strong genetic impact of shared epitope to ACPA levels after stratification of HLA-DRB1*09:01. Ann Rheum Dis. 2012;71(6):1095–7.
17. C.Terao, K.Ohmura, Y.Kochi, K.Ikari, E.Maruya, M.Katayama, et al. A large-scale association study identified multiple HLA-DRB1 alleles associated with ACPA-negative rheumatoid arthritis in Japanese subjects. Ann Rheum Dis. 2011;70(12):2134–9.
18. C.Terao, K.Ohmura, K.Ikari, Y.Kochi, E.Maruya, M.Katayama, et al. ACPA-negative RA consists of two genetically distinct subsets based on RF positivity in Japanese. PLoS One. 2012;7(7):e40067.
19. Y.Imaizumi, K.Nonaka The twinning rates by zygosity in Japan, 1975–1994. Acta Genet Med Gemellol (Roma). 1997;46(1):9–22.
20. D.Speed, G.Hemani, M.R.Johnson, D.J.Balding Improved heritability estimation from genome-wide SNPs. Am J Hum Genet. 2012;91(6):1011–21.
21. Y.Kochi, Y.Okada, A.Suzuki, K.Ikari, C.Terao, A.Takahashi, et al. A regulatory variant in CCR6 is associated with rheumatoid arthritis susceptibility. Nat Genet. 2010;42(6):515–19.
22. C.Terao, K.Yano, K.Ikari, M.Furu, N.Yamakawa, S.Yoshida,. A main contribution of DRB1*04:05 among shared epitope and involvement of 57th DRB1 amino acid in association with joint destruction in ACPA(+) RA. Arthritis Rheumatol. 2015;67(7):1744–50.