Mutua Florence, Su Ruey-Chyi, Ball Terry Blake, Kiazyk Sandra
Department of Medical Microbiology and Infectious Diseases, Max Rady College of Medicine, University of Manitoba, Room 543-745 Bannatyne Avenue, Winnipeg, MB R3E 0J9, Canada.
Department of Medical Microbiology and Immunology, Kenyatta National Hospital Campus, University of Nairobi, Nairobi P.O. Box 30197-00100, Kenya.
Infect Dis Rep. 2025 Jul 8;17(4):81. doi: 10.3390/idr17040081.
The identification of a type I interferon-induced transcriptomic signature in active tuberculosis suggests a potential role for these interferons in the pathogenesis of tuberculosis. Comorbidities such as human immunodeficiency virus, diabetes, systemic lupus erythematosus, end-stage renal disease, and coronavirus disease are epidemiologically linked to an increased risk for reactivation of latent tuberculosis infection. Notably, type I interferons are also implicated in the pathogenesis of these conditions, with a recognizable type I interferon transcriptomic signature. The mechanisms by which type I interferons in tuberculosis-risk-associated comorbidities may drive the progression of tuberculosis or maintenance of latent infection however remain largely unknown. This review summarizes the existing literature on the increased association between type I interferons, focusing on interferon-α and -β, and the heightened risk of tuberculosis reactivation. It also underscores the similarities in the immunopathogenesis of these comorbidities. A better understanding of these mechanisms is essential to guide the development of host-directed interferon therapies and improving diagnostic biomarkers in infection.
在活动性结核病中鉴定出I型干扰素诱导的转录组特征，提示这些干扰素在结核病发病机制中可能发挥作用。诸如人类免疫缺陷病毒、糖尿病、系统性红斑狼疮、终末期肾病和冠状病毒病等合并症在流行病学上与潜伏性结核感染再激活风险增加相关。值得注意的是，I型干扰素也与这些疾病的发病机制有关，具有可识别的I型干扰素转录组特征。然而，与结核病风险相关的合并症中的I型干扰素驱动结核病进展或维持潜伏感染的机制仍 largely未知。本综述总结了关于I型干扰素（主要关注干扰素-α和-β）与结核病再激活风险增加之间更强关联的现有文献。它还强调了这些合并症在免疫发病机制上的相似性。更好地理解这些机制对于指导宿主导向的干扰素疗法的开发以及改善感染中的诊断生物标志物至关重要。
