Center for Biologics Evaluation and Research, Food and Drug Administration, Silver Spring, Maryland, United States of America.
Department of Microbiology and Physiological Systems, UMass Chan Medical School, Worcester, Massachusetts, United States of America.
PLoS Pathog. 2024 Mar 7;20(3):e1012069. doi: 10.1371/journal.ppat.1012069. eCollection 2024 Mar.
Mycobacterium tuberculosis (M.tb.) infection leads to over 1.5 million deaths annually, despite widespread vaccination with BCG at birth. Causes for the ongoing tuberculosis endemic are complex and include the failure of BCG to protect many against progressive pulmonary disease. Host genetics is one of the known factors implicated in susceptibility to primary tuberculosis, but less is known about the role that host genetics plays in controlling host responses to vaccination against M.tb. Here, we addressed this gap by utilizing Diversity Outbred (DO) mice as a small animal model to query genetic drivers of vaccine-induced protection against M.tb. DO mice are a highly genetically and phenotypically diverse outbred population that is well suited for fine genetic mapping. Similar to outcomes in people, our previous studies demonstrated that DO mice have a wide range of disease outcomes following BCG vaccination and M.tb. challenge. In the current study, we used a large population of BCG-vaccinated/M.tb.-challenged mice to perform quantitative trait loci mapping of complex infection traits; these included lung and spleen M.tb. burdens, as well as lung cytokines measured at necropsy. We found sixteen chromosomal loci associated with complex infection traits and cytokine production. QTL associated with bacterial burdens included a region encoding major histocompatibility antigens that are known to affect susceptibility to tuberculosis, supporting validity of the approach. Most of the other QTL represent novel associations with immune responses to M.tb. and novel pathways of cytokine regulation. Most importantly, we discovered that protection induced by BCG is a multigenic trait, in which genetic loci harboring functionally-distinct candidate genes influence different aspects of immune responses that are crucial collectively for successful protection. These data provide exciting new avenues to explore and exploit in developing new vaccines against M.tb.
结核分枝杆菌(M.tb.)感染每年导致超过 150 万人死亡,尽管在出生时广泛接种卡介苗(BCG)。导致结核病持续存在的原因很复杂,包括 BCG 未能保护许多人免受进行性肺病的侵害。宿主遗传学是导致原发性结核病易感性的已知因素之一,但宿主遗传学在控制宿主对 M.tb 疫苗接种的反应方面所起的作用知之甚少。在这里,我们利用多样性杂交(DO)小鼠作为一种小动物模型来研究控制 M.tb 疫苗诱导保护的宿主遗传驱动因素,从而填补了这一空白。DO 小鼠是一种高度遗传和表型多样化的杂交种群,非常适合精细的遗传作图。与人类的结果相似,我们之前的研究表明,DO 小鼠在接种 BCG 和接种 M.tb 后,疾病的结果有很大的差异。在当前的研究中,我们使用了大量接种 BCG/接种 M.tb 挑战的小鼠,对复杂感染特征进行了数量性状基因座作图;这些特征包括肺部和脾脏的 M.tb 负担,以及尸检时测量的肺部细胞因子。我们发现了与复杂感染特征和细胞因子产生相关的 16 个染色体位点。与细菌负担相关的 QTL 包括编码主要组织相容性抗原的区域,这些抗原已知会影响结核病的易感性,支持该方法的有效性。大多数其他 QTL 代表与 M.tb 免疫反应和细胞因子调节的新途径的新关联。最重要的是,我们发现 BCG 诱导的保护是一种多基因特征,其中含有功能不同的候选基因的遗传位点影响着免疫反应的不同方面,这些方面对于成功的保护是至关重要的。这些数据为探索和利用开发针对 M.tb 的新型疫苗提供了令人兴奋的新途径。