McGarry F, Neilly J, Anderson N, Sturrock R, Field M
Centre for Rheumatic Diseases, University Department of Medicine, Glasgow Royal Infirmary, 10 Alexandra Parade, Glasgow G31 2ER, UK.
Rheumatology (Oxford). 2001 Dec;40(12):1359-64. doi: 10.1093/rheumatology/40.12.1359.
Genetic factors that predispose individuals to ankylosing spondylitis (AS) are not fully understood, but are unlikely to be restricted to HLA-B27. Proinflammatory cytokines are implicated in the development of sacroiliitis. We have examined the allele frequencies of three polymorphic sites in the interleukin (IL)-1 genes in AS patients to investigate whether genetic regulation of IL-1 production could be implicated in AS pathogenesis.
DNA from 188 AS patients, 115 healthy controls and 81 HLA-B27-positive healthy controls, all from the West of Scotland, were examined with the polymerase chain reaction in a case-controlled study. Polymorphic sites in genes of the IL-1 family were examined, including the 86-base pair variable number tandem repeat within intron 2 of the IL-1Ra gene, and the restriction fragment length polymorphisms at positions -889 in the IL-1alpha gene and -511 in the IL-1beta gene.
No significant differences were seen at the polymorphic alleles in the IL-1alpha and IL-1beta genes, but there was a significant increase in the carriage of allele 2 in the IL-1Ra in the AS patients compared with local controls (16 vs 8%, odds ratio 2.3, 95% confidence interval 1.2-4.4, P=0.01).
This report of an association with a polymorphic site within the IL-1 locus and AS suggests that genes other than B27 may well be involved in the pathogenesis of AS.
虽然导致个体易患强直性脊柱炎(AS)的遗传因素尚未完全明确,但不太可能仅限于HLA - B27。促炎细胞因子与骶髂关节炎的发生有关。我们检测了AS患者白细胞介素(IL)-1基因中三个多态性位点的等位基因频率,以研究IL - 1产生的遗传调控是否与AS发病机制有关。
在一项病例对照研究中,采用聚合酶链反应检测了来自苏格兰西部的188例AS患者、115名健康对照者和81名HLA - B27阳性健康对照者的DNA。检测了IL - 1家族基因中的多态性位点,包括IL - 1Ra基因内含子2中86个碱基对的可变数目串联重复序列,以及IL - 1α基因 - 889位和IL - 1β基因 - 511位的限制性片段长度多态性。
IL - 1α和IL - 1β基因的多态性等位基因未见显著差异,但与当地对照相比,AS患者中IL - 1Ra基因2等位基因的携带率显著增加(16%对8%,优势比2.3,95%置信区间1.2 - 4.4,P = 0.01)。
本报告显示IL - 1基因座内的一个多态性位点与AS有关,这表明除B27外的其他基因很可能参与了AS的发病机制。