Mistry Vanisha, Bockett Nicholas A, Levine Adam P, Mirza Muddassar M, Hunt Karen A, Ciclitira Paul J, Hummerich Holger, Neuhausen Susan L, Simpson Michael A, Plagnol Vincent, van Heel David A
Blizard Institute, Barts and The London School of Medicine and Dentistry, 4 Newark Street, London E1 2AT, United Kingdom.
Division of Medicine, University College London, London, WC1E 6JF, United Kingdom.
PLoS One. 2015 Jan 30;10(1):e0116845. doi: 10.1371/journal.pone.0116845. eCollection 2015.
Coeliac disease (CeD) is a highly heritable common autoimmune disease involving chronic small intestinal inflammation in response to dietary wheat. The human leukocyte antigen (HLA) region, and 40 newer regions identified by genome wide association studies (GWAS) and dense fine mapping, account for ∼40% of the disease heritability. We hypothesized that in pedigrees with multiple individuals with CeD rare [minor allele frequency (MAF) <0.5%] mutations of larger effect size (odds ratios of ∼2-5) might exist. We sequenced the exomes of 75 coeliac individuals of European ancestry from 55 multiply affected families. We selected interesting variants and genes for further follow up using a combination of: an assessment of shared variants between related subjects, a model-free linkage test, and gene burden tests for multiple, potentially causal, variants. We next performed highly multiplexed amplicon resequencing of all RefSeq exons from 24 candidate genes selected on the basis of the exome sequencing data in 2,248 unrelated coeliac cases and 2,230 controls. 1,335 variants with a 99.9% genotyping call rate were observed in 4,478 samples, of which 939 were present in coding regions of 24 genes (Ti/Tv 2.99). 91.7% of coding variants were rare (MAF <0.5%) and 60% were novel. Gene burden tests performed on rare functional variants identified no significant associations (p<1×10(-3)) in the resequenced candidate genes. Our strategy of sequencing multiply affected families with deep follow up of candidate genes has not identified any new CeD risk mutations.
乳糜泻(CeD)是一种高度可遗传的常见自身免疫性疾病,涉及因摄入膳食小麦而引发的慢性小肠炎症。人类白细胞抗原(HLA)区域以及通过全基因组关联研究(GWAS)和密集精细定位确定的40个新区域,约占该疾病遗传度的40%。我们推测,在有多个乳糜泻患者的家系中,可能存在效应大小较大(优势比约为2至5)的罕见[次要等位基因频率(MAF)<0.5%]突变。我们对来自55个多病例家庭的75名欧洲血统的乳糜泻患者的外显子组进行了测序。我们结合以下方法选择有趣的变异和基因进行进一步随访:评估相关受试者之间的共享变异、无模型连锁检验以及对多个潜在因果变异的基因负担检验。接下来,我们对基于外显子组测序数据选择的24个候选基因的所有RefSeq外显子进行了高度多重扩增子重测序,涉及2248例无关的乳糜泻病例和2230例对照。在4478个样本中观察到1335个基因分型检出率为99.9%的变异,其中939个存在于24个基因的编码区(转换/颠换为2.99)。91.7%的编码变异是罕见的(MAF<0.5%),60%是新发现的。对罕见功能变异进行的基因负担检验在重测序的候选基因中未发现显著关联(p<1×10⁻³)。我们对多病例家庭进行测序并对候选基因进行深入随访的策略尚未发现任何新的乳糜泻风险突变。