Costantino Félicie, Mambu Mambueni Hendrick, Said-Nahal Roula, Garchon Henri-Jean, Breban Maxime
UVSQ, Inserm U1173, Infection et inflammation, Laboratory of Excellence INFLAMEX, Université Paris-Saclay, Montigny-le-Bretonneux, France.
Rheumatology Division, Ambroise Paré Hospital, Boulogne-Billancourt, France.
Front Genet. 2021 Jun 3;12:671306. doi: 10.3389/fgene.2021.671306. eCollection 2021.
Spondyloarthritis (SpA) is a chronic inflammatory disorder with a high familial aggregation, emphasizing the existence of genetic susceptibility factors. In the last decades, family-based studies have contributed to better understand the genetic background of SpA, in particular by showing that the most likely model of transmission is oligogenic with multiplicative effects. Coexistence of different SpA subtypes within families also highlighted the complex interplay between all subtypes. Several whole-genome linkage analyses using sib-pairs or multiplex families were performed in the 1990s to try to identify genetic susceptibility factors besides HLA-B27. Unfortunately, no consistent results were obtained and family-based studies have been progressively set aside in favor of case-control designs. In particular, case-control genome-wide association studies allowed the identification of more than 40 susceptibility regions. However, all these loci explain only a small fraction of disease predisposition. Several hypotheses have been advanced to account for this unexplained heritability, including rare variants involvement, leading to a renewed interest in family-based designs, which are probably more powerful in the detection of such variants. In this review, our purpose is to summarize what has been learned to date regarding SpA genetics from family-based studies, with a special focus on recent identification of rare associated variants through next-generation sequencing studies.
脊柱关节炎(SpA)是一种具有高度家族聚集性的慢性炎症性疾病,这凸显了遗传易感因素的存在。在过去几十年中,基于家系的研究有助于更好地理解SpA的遗传背景,特别是通过表明最可能的遗传模式是具有累加效应的寡基因遗传。家族中不同SpA亚型的共存也凸显了所有亚型之间复杂的相互作用。20世纪90年代进行了几项使用同胞对或多重家系的全基因组连锁分析,试图识别除HLA - B27之外的遗传易感因素。不幸的是,没有获得一致的结果,基于家系的研究逐渐被搁置,转而青睐病例对照设计。特别是,病例对照全基因组关联研究使得能够识别出40多个易感区域。然而,所有这些基因座仅解释了疾病易感性的一小部分。已经提出了几种假设来解释这种无法解释的遗传力,包括罕见变异的参与,这导致人们对基于家系的设计重新产生兴趣,因为这种设计在检测此类变异方面可能更具效力。在这篇综述中,我们的目的是总结迄今为止从基于家系的研究中所了解到的关于SpA遗传学的知识,特别关注通过下一代测序研究最近鉴定出的罕见相关变异。