Tumor necrosis factor gene polymorphisms in ankylosing spondylitis

被引:0
作者
Fraile, A
Nieto, A
Beraún, Y
Vinasco, J
Matarán, L
Martín, J
机构
[1] CSIC, Inst Parasitol & Biomed Lopez Neyra, Granada 18001, Spain
[2] Hosp Virgen Nieves, Serv Reumatol, Granada, Spain
来源
TISSUE ANTIGENS | 1998年 / 51卷 / 04期
关键词
ankylosing spondylitis; HLA-B*27; TNF;
D O I
暂无
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Despite the strength of the association of ankylosing spondylitis (AS) with HLA-B27, other genetic elements could play a possible role in the pathophysiology of AS. In view of its gene location, in the proximity of the HLA-B locus, and biological effects, tumor necrosis factor (TNF) genes are potential candidates for additive susceptibility factors to AS. TNF alpha and TNF beta genotypes were analyzed by PCR-RFLP in 57 patients with AS, 102 random controls and 30 HLA-B*27-positive controls. No significant differences of TNF alpha promoter variations at position -308 and -238 were found in AS patients in comparison with controls. The -244 polymorphism was not detected in our population. The TNF beta genotype frequency was significantly different between AS patients and random controls, However, when the distribution of the TNF beta genotype was compared in B*27-positive AS patients and controls, these differences disappeared. In addition, we demonstrated that the TNF beta*1 was in strong linkage disequilibrium with the B*27 allele, which may explain the differences observed for the TNF beta genotype among AS patients and random controls Our data suggest that the polymorphisms of TNF alpha and TNF beta genes do not have an independent effect on AS susceptibility.
引用
收藏
页码:386 / 390
页数:5
相关论文
共 18 条
[1]  
ABRAHAM LJ, 1993, CLIN EXP IMMUNOL, V92, P14
[2]   USE OF IMMUNOHISTOLOGIC AND IN-SITU HYBRIDIZATION TECHNIQUES IN THE EXAMINATION OF SACROILIAC JOINT BIOPSY SPECIMENS FROM PATIENTS WITH ANKYLOSING-SPONDYLITIS [J].
BRAUN, J ;
BOLLOW, M ;
NEURE, L ;
SEIPELT, E ;
SEYREKBASAN, F ;
HERBST, H ;
EGGENS, U ;
DISTLER, A ;
SIEPER, J .
ARTHRITIS AND RHEUMATISM, 1995, 38 (04) :499-505
[3]  
DYER P, 1994, HLA DIS, P93
[4]  
GALBRAITH GMP, 1995, HUM GENET, V96, P433
[5]  
GRATACOS J, 1994, BRIT J RHEUMATOL, V33, P927
[6]   ALLELIC VARIATION IN THE TNF-BETA GENE DOES NOT EXPLAIN THE LOW TNF-BETA RESPONSE IN PATIENTS WITH PRIMARY BILIARY-CIRRHOSIS [J].
MESSER, G ;
SPENGLER, U ;
JUNG, MC ;
HONOLD, G ;
EISENBURG, J ;
SCHOLZ, S ;
ALBERT, ED ;
PAPE, GR ;
RIETHMULLER, G ;
WEISS, EH .
SCANDINAVIAN JOURNAL OF IMMUNOLOGY, 1991, 34 (06) :735-740
[7]   HLA-B*27 typing by PCR-restriction fragment length polymorphism [J].
Nieto, A ;
Fraile, A ;
Vinasco, J ;
Martin, J .
TISSUE ANTIGENS, 1997, 49 (03) :283-286
[8]   ASSOCIATION OF TUMOR-NECROSIS-FACTOR (TNF) AND CLASS-II MAJOR HISTOCOMPATIBILITY COMPLEX ALLELES WITH THE SECRETION OF TNF-ALPHA AND TNF-BETA BY HUMAN MONONUCLEAR-CELLS - A POSSIBLE LINK TO INSULIN-DEPENDENT DIABETES-MELLITUS [J].
POCIOT, F ;
BRIANT, L ;
JONGENEEL, CV ;
MOLVIG, J ;
WORSAAE, H ;
ABBAL, M ;
THOMSEN, M ;
NERUP, J ;
CAMBONTHOMSEN, A .
EUROPEAN JOURNAL OF IMMUNOLOGY, 1993, 23 (01) :224-231
[9]   FUNCTIONAL-ANALYSIS OF A NEW POLYMORPHISM IN THE HUMAN TNF-ALPHA GENE PROMOTER [J].
POCIOT, F ;
DALFONSO, S ;
COMPASSO, S ;
SCORZA, R ;
RICHIARDI, PM .
SCANDINAVIAN JOURNAL OF IMMUNOLOGY, 1995, 42 (04) :501-504
[10]  
REPO H, 1988, CLIN EXP IMMUNOL, V72, P410