CTLA4 gene polymorphism and autoimmunity

被引:220
作者
Gough, SCL
Walker, LSK
Sansom, DM
机构
[1] Univ Birmingham, Inst Biomed Res, Div Med Sci, Birmingham B9 5SS, W Midlands, England
[2] Univ Birmingham, Inst Biomed Res, MRC, Ctr Immune Regulat, Birmingham B9 5SS, W Midlands, England
基金
英国惠康基金;
关键词
D O I
10.1111/j.0105-2896.2005.00249.x
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
CD28 and cytotoxic T-lymphocyte antigen-4 (CTLA4) are two receptors that have critical but opposing functions in T-cell stimulation. CD28 promotes a number of T-cell activities, whereas in contrast CTLA4 is an essential inhibitor of T-cell responses. Because of its inhibitory role, CTLA4 is a strong candidate susceptibility gene in autoimmunity and several studies suggest disease-associated polymorphisms. In this review, we discuss recent progress in relating CTLA4 polymorphisms to disease susceptibility and consider the putative mechanisms by which CTLA4 may act to inhibit autoimmunity.
引用
收藏
页码:102 / 115
页数:14
相关论文
共 122 条
[11]   The inhibitory function of CTLA-4 does not require its tyrosine phosphorylation [J].
Baroja, ML ;
Luxenberg, D ;
Chau, T ;
Ling, V ;
Strathdee, CA ;
Carreno, BM ;
Madrenas, J .
JOURNAL OF IMMUNOLOGY, 2000, 164 (01) :49-55
[12]   Evidence for CTLA4 as a susceptibility gene for systemic lupus erythematosus [J].
Barreto, M ;
Santos, E ;
Ferreira, R ;
Fesel, C ;
Fontes, MF ;
Pereira, C ;
Martins, B ;
Andreia, R ;
Viana, JF ;
Crespo, F ;
Vasconcelos, C ;
Ferreira, C ;
Vicente, AM .
EUROPEAN JOURNAL OF HUMAN GENETICS, 2004, 12 (08) :620-626
[13]   Polymorphisms in the cytotoxic T lymphocyte antigen-4 gene region confer susceptibility to Addison's disease [J].
Blomhoff, A ;
Lie, BA ;
Myhre, AG ;
Kemp, EH ;
Weetman, AP ;
Akselsen, HE ;
Huseby, ES ;
Undlien, DE .
JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, 2004, 89 (07) :3474-3476
[14]   CTLA-4 promoter variants in patients with Graves' disease and Hashimoto's thyroiditis [J].
Braun, J ;
Donner, H ;
Siegmund, T ;
Walfish, PG ;
Usadel, KH ;
Badenhoop, K .
TISSUE ANTIGENS, 1998, 51 (05) :563-566
[15]   A NEW MEMBER OF THE IMMUNOGLOBULIN SUPERFAMILY - CTLA-4 [J].
BRUNET, JF ;
DENIZOT, F ;
LUCIANI, MF ;
ROUXDOSSETO, M ;
SUZAN, M ;
MATTEI, MG ;
GOLSTEIN, P .
NATURE, 1987, 328 (6127) :267-270
[16]  
Chuang E, 1997, J IMMUNOL, V159, P144
[17]   The interaction properties of costimulatory molecules revisited [J].
Collins, AV ;
Brodie, DW ;
Gilbert, RJC ;
Iaboni, A ;
Manso-Sancho, R ;
Walse, B ;
Stuart, DI ;
van der Merwe, PA ;
Davis, SJ .
IMMUNITY, 2002, 17 (02) :201-210
[18]   A second-generation screen of the human genome for susceptibility to insulin-dependent diabetes mellitus [J].
Concannon, P ;
Gogolin-Ewens, KJ ;
Hinds, DA ;
Wapelhorst, B ;
Morrison, VA ;
Stirling, B ;
Mitra, M ;
Farmer, J ;
Williams, SR ;
Cox, NJ ;
Bell, GI ;
Risch, N ;
Spielman, RS .
NATURE GENETICS, 1998, 19 (03) :292-296
[19]   The 3′ untranslated region of messenger RNA:: A molecular 'hotspot' for pathology? [J].
Conne, B ;
Stutz, A ;
Vassalli, JD .
NATURE MEDICINE, 2000, 6 (06) :637-641
[20]   LINKAGE DISEQUILIBRIUM MAPPING OF A TYPE-1 DIABETES SUSCEPTIBILITY GENE (IDDM7) TO CHROMOSOME 2Q31-Q33 [J].
COPEMAN, JB ;
CUCCA, F ;
HEARNE, CM ;
CORNALL, RJ ;
REED, PW ;
RONNINGEN, KS ;
UNDLIEN, DE ;
NISTICO, L ;
BUZZETTI, R ;
TOSI, R ;
POCIOT, F ;
NERUP, J ;
CORNELIS, F ;
BARNETT, AH ;
BAIN, SC ;
TODD, JA .
NATURE GENETICS, 1995, 9 (01) :80-85