Mauracher Andrea A, Henrickson Sarah E
Division of Allergy and Immunology, Department of Pediatrics, Children's Hospital of Philadelphia, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, United States.
Department of Microbiology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, United States.
Front Syst Biol. 2022;2. doi: 10.3389/fsysb.2022.910243. Epub 2022 Jul 18.
Inborn errors of immunity (IEI) are monogenic disorders that can cause diverse symptoms, including recurrent infections, autoimmunity and malignancy. While many factors have contributed, the increased availability of next-generation sequencing has been central in the remarkable increase in identification of novel monogenic IEI over the past years. Throughout this phase of disease discovery, it has also become evident that a given gene variant does not always yield a consistent phenotype, while variants in seemingly disparate genes can lead to similar clinical presentations. Thus, it is increasingly clear that the clinical phenotype of an IEI patient is not defined by genetics alone, but is also impacted by a myriad of factors. Accordingly, we need methods to amplify our current diagnostic algorithms to better understand mechanisms underlying the variability in our patients and to optimize treatment. In this review, we will explore how systems immunology can contribute to optimizing both diagnosis and treatment of IEI patients by focusing on identifying and quantifying key dysregulated pathways. To improve mechanistic understanding in IEI we must deeply evaluate our rare IEI patients using multimodal strategies, allowing both the quantification of altered immune cell subsets and their functional evaluation. By studying representative controls and patients, we can identify causative pathways underlying immune cell dysfunction and move towards functional diagnosis. Attaining this deeper understanding of IEI will require a stepwise strategy. First, we need to broadly apply these methods to IEI patients to identify patterns of dysfunction. Next, using multimodal data analysis, we can identify key dysregulated pathways. Then, we must develop a core group of simple, effective functional tests that target those pathways to increase efficiency of initial diagnostic investigations, provide evidence for therapeutic selection and contribute to the mechanistic evaluation of genetic results. This core group of simple, effective functional tests, targeting key pathways, can then be equitably provided to our rare patients. Systems biology is thus poised to reframe IEI diagnosis and therapy, fostering research today that will provide streamlined diagnosis and treatment choices for our rare and complex patients in the future, as well as providing a better understanding of basic immunology.
遗传性免疫缺陷病(IEI)是单基因疾病,可导致多种症状,包括反复感染、自身免疫和恶性肿瘤。尽管有许多因素起了作用,但在过去几年中,新一代测序技术的日益普及是新发现的单基因IEI显著增加的核心因素。在疾病发现的这个阶段,也越来越明显的是,给定的基因变异并不总是产生一致的表型,而看似不同的基因中的变异可能导致相似的临床表现。因此,越来越清楚的是,IEI患者的临床表型不仅由遗传学决定,还受到众多因素的影响。因此,我们需要方法来扩展我们当前的诊断算法,以更好地理解患者变异背后的机制并优化治疗。在这篇综述中,我们将探讨系统免疫学如何通过专注于识别和量化关键的失调途径,为优化IEI患者的诊断和治疗做出贡献。为了提高对IEI的机制理解,我们必须使用多模式策略深入评估我们的罕见IEI患者,既可以量化免疫细胞亚群的改变,也可以对其进行功能评估。通过研究代表性的对照和患者,我们可以识别免疫细胞功能障碍背后的致病途径,并朝着功能诊断迈进。要对IEI有更深入的理解,需要一个逐步推进的策略。首先,我们需要将这些方法广泛应用于IEI患者,以识别功能障碍模式。接下来,使用多模式数据分析,我们可以识别关键的失调途径。然后,我们必须开发一组针对这些途径的简单有效的核心功能测试,以提高初始诊断调查的效率,为治疗选择提供证据,并有助于对基因结果进行机制评估。然后,可以将这组针对关键途径的简单有效的核心功能测试公平地提供给我们的罕见病患者。因此,系统生物学有望重塑IEI的诊断和治疗,推动当今的研究,为我们未来的罕见病和复杂病患者提供简化的诊断和治疗选择,并更好地理解基础免疫学。