Association of human leukocyte antigen with interstitial lung disease in rheumatoid arthritis: a protective role for shared epitope.
Association of human leukocyte antigen with interstitial lung disease in rheumatoid arthritis: a protective role for shared epitope.
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DOI:
10.1371/journal.pone.0033133
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发表时间:
2012
期刊:
影响因子:
3.7
通讯作者:
Tohma S
中科院分区:
文献类型:
--
作者:
Furukawa H;Oka S;Shimada K;Sugii S;Ohashi J;Matsui T;Ikenaka T;Nakayama H;Hashimoto A;Takaoka H;Arinuma Y;Okazaki Y;Futami H;Komiya A;Fukui N;Nakamura T;Migita K;Suda A;Nagaoka S;Tsuchiya N;Tohma S
Interstitial Lung Disease (ILD) is frequently associated with Rheumatoid Arthritis (RA) as one of extra-articular manifestations. Many studies for Human Leukocyte Antigen (HLA) allelic association with RA have been reported, but few have been validated in an RA subpopulation with ILD. In this study, we investigated the association of HLA class II alleles with ILD in RA. An association study was conducted on HLA-DRB1, DQB1, and DPB1 in 450 Japanese RA patients that were or were not diagnosed with ILD, based on the findings of computed tomography images of the chest. Unexpectedly, HLA-DRB1*04 (corrected P [Pc] = 0.0054, odds ratio [OR] 0.57), shared epitope (SE) (P = 0.0055, OR 0.66) and DQB1*04 (Pc = 0.0036, OR 0.57) were associated with significantly decreased risk of ILD. In contrast, DRB1*16 (Pc = 0.0372, OR 15.21), DR2 serological group (DRB1*15 and *16 alleles) (P = 0.0020, OR 1.75) and DQB1*06 (Pc = 0.0333, OR 1.57, respectively) were significantly associated with risk of ILD. HLA-DRB1 SE was associated with reduced, while DR2 serological group (DRB1*15 and *16) with increased, risk for ILD in Japanese patients with RA.
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影响因子:
4.9
作者:
Turesson C;Schaid DJ;Weyand CM;Jacobsson LT;Goronzy JJ;Petersson IF;Sturfelt G;Nyhäll-Wåhlin BM;Truedsson L;Dechant SA;Matteson EL
通讯作者:
Matteson EL
DOI:
10.1016/0197-2456(86)90046-2
发表时间:
1986-09-01
期刊:
CONTROLLED CLINICAL TRIALS
影响因子:
--
作者:
DERSIMONIAN, R;LAIRD, N
通讯作者:
LAIRD, N
影响因子:
5.3
作者:
Falfán-Valencia, R;Camarena, A;Selman, M
通讯作者:
Selman, M
影响因子:
--
作者:
Sirikong, M;Tsuchiya, N;Tokunaga, K
通讯作者:
Tokunaga, K
影响因子:
19.7
作者:
Webb, WR
通讯作者:
Webb, WR