THE ROLE OF T-CELL RECEPTOR-BETA CHAIN GENES IN SUSCEPTIBILITY TO RHEUMATOID-ARTHRITIS

被引:25
作者
MCDERMOTT, M
KASTNER, DL
HOLLOMAN, JD
SCHMIDTWOLF, G
LUNDBERG, AS
SINHA, AA
HSU, C
CASHIN, P
MOLLOY, MG
MULCAHY, B
OGARA, F
MCCONNELL, FI
ADAMS, C
KHAN, MA
WOLFE, F
RUBIN, LA
CLEGG, DO
HUSEBYE, D
AMOS, CI
WARD, RH
MCDEVITT, HO
机构
[1] NIAMS, ARTHRIT & RHEUMATISM BRANCH, BETHESDA, MD USA
[2] STANFORD UNIV, STANFORD, CA 94305 USA
[3] CASE WESTERN RESERVE UNIV, CLEVELAND, OH 44106 USA
[4] UNIV KANSAS, WICHITA, KS USA
[5] UNIV TORONTO, WOMENS COLL HOSP, TORONTO, ON, CANADA
[6] UNIV UTAH, SCH MED, SALT LAKE CITY, UT USA
[7] UNIV TEXAS, MD ANDERSON CANC CTR, HOUSTON, TX USA
来源
ARTHRITIS AND RHEUMATISM | 1995年 / 38卷 / 01期
关键词
D O I
10.1002/art.1780380114
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Objective. To evaluate the role of the T cell receptor beta chain locus (TCRB) in genetic susceptibility to rheumatoid arthritis (RA). Methods. Twenty-eight multiplex RA families were recruited from 3 rheumatology outpatient departments. All members were genotyped for a highly informative microsatellite (V(beta)6.7), a V(beta)12.2 SSCP marker, and a biallelic C-beta restriction fragment length polymorphism. Data were analyzed by the SIBPAL program to assess identity-by-descent in affected sib-pairs. Results. Using the V(beta)12.2 marker, there was suggestive evidence of increased sib-pair sharing (P = 0.005) in affected offspring (a P value of 0.001 is generally taken to establish linkage). Data for V(beta)6.7 and C-beta yielded significance levels of 0.06 and 0.19, respectively. Conclusion. These data suggest that a gene in or linked to the TCRB complex may confer genetic susceptibility to RA in these families. Confirmation in a larger panel of families is required.
引用
收藏
页码:91 / 95
页数:5
相关论文
共 13 条
[1]  
ABDALLA JA, 1992, AM J HUM GENET, V51, P579
[2]   THE AMERICAN-RHEUMATISM-ASSOCIATION 1987 REVISED CRITERIA FOR THE CLASSIFICATION OF RHEUMATOID-ARTHRITIS [J].
ARNETT, FC ;
EDWORTHY, SM ;
BLOCH, DA ;
MCSHANE, DJ ;
FRIES, JF ;
COOPER, NS ;
HEALEY, LA ;
KAPLAN, SR ;
LIANG, MH ;
LUTHRA, HS ;
MEDSGER, TA ;
MITCHELL, DM ;
NEUSTADT, DH ;
PINALS, RS ;
SCHALLER, JG ;
SHARP, JT ;
WILDER, RL ;
HUNDER, GG .
ARTHRITIS AND RHEUMATISM, 1988, 31 (03) :315-324
[3]  
BLACKWELDER W C, 1985, Genetic Epidemiology, V2, P85, DOI 10.1002/gepi.1370020109
[4]   HAPLOTYPING THE HUMAN T-CELL RECEPTOR BETA-CHAIN GENE-COMPLEX BY USE OF RESTRICTION-FRAGMENT-LENGTH-POLYMORPHISMS [J].
CHARMLEY, P ;
CHAO, A ;
CONCANNON, P ;
HOOD, L ;
GATTI, RA .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1990, 87 (12) :4823-4827
[5]  
CORNELIS FB, 1993, ARTHRITIS RHEUM, V36, pS82
[6]   SILENT ALLELIC VARIANTS OF A T-CELL RECEPTOR V-BETA-12 GENE ARE PRESENT IN DIVERSE HUMAN-POPULATIONS [J].
DAY, CE ;
ZHAO, TM ;
ROBINSON, MA .
HUMAN IMMUNOLOGY, 1992, 34 (03) :196-202
[7]   DIFFERENCES IN T-CELL RECEPTOR RESTRICTION-FRAGMENT-LENGTH-POLYMORPHISMS IN PATIENTS WITH RHEUMATOID-ARTHRITIS [J].
FUNKHOUSER, SW ;
CONCANNON, P ;
CHARMLEY, P ;
VREDEVOE, DL ;
HOOD, L .
ARTHRITIS AND RHEUMATISM, 1992, 35 (04) :465-471
[8]   MOLECULAR DIVERSITY OF HLA-DR4 HAPLOTYPES [J].
GREGERSEN, PK ;
MING, S ;
SONG, QL ;
MERRYMAN, P ;
DEGAR, S ;
SEKI, T ;
MACCARI, J ;
GOLDBERG, D ;
MURPHY, H ;
SCHWENZER, J ;
CHANG, YW ;
WINCHESTER, RJ ;
NEPOM, GT ;
SILVER, J .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1986, 83 (08) :2642-2646
[9]   T-CELL RECEPTOR V-BETA GENE BIAS IN RHEUMATOID-ARTHRITIS [J].
JENKINS, RN ;
NIKAEIN, A ;
ZIMMERMANN, A ;
MEEK, K ;
LIPSKY, PE .
JOURNAL OF CLINICAL INVESTIGATION, 1993, 92 (06) :2688-2701
[10]   INVESTIGATING THE HLA COMPONENT IN RHEUMATOID-ARTHRITIS - AN ADDITIVE (DOMINANT) MODE OF INHERITANCE IS REJECTED, A RECESSIVE MODE IS PREFERRED [J].
RIGBY, AS ;
SILMAN, AJ ;
VOELM, L ;
GREGORY, JC ;
OLLIER, WER ;
KHAN, MA ;
NEPOM, GT ;
THOMSON, G .
GENETIC EPIDEMIOLOGY, 1991, 8 (03) :153-175