"共享基因组片段分析表明,MHC I 类和 III 类分子是幼年特发性关节炎的遗传风险因素。

IF 3.3 Q2 GENETICS & HEREDITY
HGG Advances Pub Date : 2024-04-11 Epub Date: 2024-02-18 DOI:10.1016/j.xhgg.2024.100277
Cecile N Avery, Nicole D Russell, Cody J Steely, Aimee O Hersh, John F Bohnsack, Sampath Prahalad, Lynn B Jorde
{"title":"\"共享基因组片段分析表明,MHC I 类和 III 类分子是幼年特发性关节炎的遗传风险因素。","authors":"Cecile N Avery, Nicole D Russell, Cody J Steely, Aimee O Hersh, John F Bohnsack, Sampath Prahalad, Lynn B Jorde","doi":"10.1016/j.xhgg.2024.100277","DOIUrl":null,"url":null,"abstract":"<p><p>Juvenile idiopathic arthritis (JIA) is a complex rheumatic disease encompassing several clinically defined subtypes of varying severity. The etiology of JIA remains largely unknown, but genome-wide association studies (GWASs) have identified up to 22 genes associated with JIA susceptibility, including a well-established association with HLA-DRB1. Continued investigation of heritable risk factors has been hindered by disease heterogeneity and low disease prevalence. In this study, we utilized shared genomic segments (SGS) analysis on whole-genome sequencing of 40 cases from 12 multi-generational pedigrees significantly enriched for JIA. Subsets of cases are connected by a common ancestor in large extended pedigrees, increasing the power to identify disease-associated loci. SGS analysis identifies genomic segments shared among disease cases that are likely identical by descent and anchored by a disease locus. This approach revealed statistically significant signals for major histocompatibility complex (MHC) class I and class III alleles, particularly HLA-A∗02:01, which was observed at a high frequency among cases. Furthermore, we identified an additional risk locus at 12q23.2-23.3, containing genes primarily expressed by naive B cells, natural killer cells, and monocytes. The recognition of additional risk beyond HLA-DRB1 provides a new perspective on immune cell dynamics in JIA. These findings contribute to our understanding of JIA and may guide future research and therapeutic strategies.</p>","PeriodicalId":34530,"journal":{"name":"HGG Advances","volume":null,"pages":null},"PeriodicalIF":3.3000,"publicationDate":"2024-04-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10918567/pdf/","citationCount":"0","resultStr":"{\"title\":\"Shared genomic segments analysis identifies MHC class I and class III molecules as genetic risk factors for juvenile idiopathic arthritis.\",\"authors\":\"Cecile N Avery, Nicole D Russell, Cody J Steely, Aimee O Hersh, John F Bohnsack, Sampath Prahalad, Lynn B Jorde\",\"doi\":\"10.1016/j.xhgg.2024.100277\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Juvenile idiopathic arthritis (JIA) is a complex rheumatic disease encompassing several clinically defined subtypes of varying severity. The etiology of JIA remains largely unknown, but genome-wide association studies (GWASs) have identified up to 22 genes associated with JIA susceptibility, including a well-established association with HLA-DRB1. Continued investigation of heritable risk factors has been hindered by disease heterogeneity and low disease prevalence. In this study, we utilized shared genomic segments (SGS) analysis on whole-genome sequencing of 40 cases from 12 multi-generational pedigrees significantly enriched for JIA. Subsets of cases are connected by a common ancestor in large extended pedigrees, increasing the power to identify disease-associated loci. SGS analysis identifies genomic segments shared among disease cases that are likely identical by descent and anchored by a disease locus. This approach revealed statistically significant signals for major histocompatibility complex (MHC) class I and class III alleles, particularly HLA-A∗02:01, which was observed at a high frequency among cases. Furthermore, we identified an additional risk locus at 12q23.2-23.3, containing genes primarily expressed by naive B cells, natural killer cells, and monocytes. The recognition of additional risk beyond HLA-DRB1 provides a new perspective on immune cell dynamics in JIA. These findings contribute to our understanding of JIA and may guide future research and therapeutic strategies.</p>\",\"PeriodicalId\":34530,\"journal\":{\"name\":\"HGG Advances\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":3.3000,\"publicationDate\":\"2024-04-11\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10918567/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"HGG Advances\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.1016/j.xhgg.2024.100277\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2024/2/18 0:00:00\",\"PubModel\":\"Epub\",\"JCR\":\"Q2\",\"JCRName\":\"GENETICS & HEREDITY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"HGG Advances","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1016/j.xhgg.2024.100277","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2024/2/18 0:00:00","PubModel":"Epub","JCR":"Q2","JCRName":"GENETICS & HEREDITY","Score":null,"Total":0}
引用次数: 0

摘要

幼年特发性关节炎(JIA)是一种复杂的风湿性疾病,包括几种临床上定义的严重程度不同的亚型。JIA 的病因在很大程度上仍不清楚,但全基因组关联研究(GWAS)已发现多达 22 个与 JIA 易感性相关的基因,其中包括与 HLA-DRB1 确立的关联。疾病的异质性和低患病率阻碍了对遗传风险因素的继续研究。在这项研究中,我们利用共享基因组片段(SGS)分析法,对来自 12 个多代血统中明显富集 JIA 的 40 个病例进行了全基因组测序。在大型扩展系谱中,病例的子集由共同祖先连接,从而提高了鉴定疾病相关位点的能力。SGS 分析可确定疾病病例之间共享的基因组片段,这些片段很可能在血统上是相同的,并由疾病基因座锚定。这种方法揭示了主要组织相容性复合体(MHC)Ⅰ类和Ⅲ类等位基因的显著统计学信号,尤其是在病例中高频出现的 HLA-A*02:01。此外,我们还在 12q23.2-23.3 处发现了一个额外的风险基因座,其中包含的基因主要由幼稚 B 细胞、自然杀伤细胞和单核细胞表达。除了HLA-DRB1之外,我们还发现了一个额外的风险位点,这为我们了解JIA的免疫细胞动态提供了一个新的视角。这些发现有助于我们了解 JIA,并可指导未来的研究和治疗策略。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Shared genomic segments analysis identifies MHC class I and class III molecules as genetic risk factors for juvenile idiopathic arthritis.

Juvenile idiopathic arthritis (JIA) is a complex rheumatic disease encompassing several clinically defined subtypes of varying severity. The etiology of JIA remains largely unknown, but genome-wide association studies (GWASs) have identified up to 22 genes associated with JIA susceptibility, including a well-established association with HLA-DRB1. Continued investigation of heritable risk factors has been hindered by disease heterogeneity and low disease prevalence. In this study, we utilized shared genomic segments (SGS) analysis on whole-genome sequencing of 40 cases from 12 multi-generational pedigrees significantly enriched for JIA. Subsets of cases are connected by a common ancestor in large extended pedigrees, increasing the power to identify disease-associated loci. SGS analysis identifies genomic segments shared among disease cases that are likely identical by descent and anchored by a disease locus. This approach revealed statistically significant signals for major histocompatibility complex (MHC) class I and class III alleles, particularly HLA-A∗02:01, which was observed at a high frequency among cases. Furthermore, we identified an additional risk locus at 12q23.2-23.3, containing genes primarily expressed by naive B cells, natural killer cells, and monocytes. The recognition of additional risk beyond HLA-DRB1 provides a new perspective on immune cell dynamics in JIA. These findings contribute to our understanding of JIA and may guide future research and therapeutic strategies.

求助全文
通过发布文献求助,成功后即可免费获取论文全文。 去求助
来源期刊
HGG Advances
HGG Advances Biochemistry, Genetics and Molecular Biology-Molecular Medicine
CiteScore
4.30
自引率
4.50%
发文量
69
审稿时长
14 weeks
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信