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Journal Article Review Epublish 3 citations

PubMed: 40700327 DOI: 10.3390/idr17040081

The Role of Type I Interferons in Tuberculosis and in Tuberculosis-Risk-Associated Comorbidities.

Infect Dis Rep 17(4)

Authors: Florence Mutua, Ruey-Chyi Su, Terry Blake Ball, Sandra Kiazyk

Affiliations

  • 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.
  • National Sexually Transmitted and Bloodborne Infections Laboratory Division, JC Wilt Infectious Diseases Research Centre, Public Health Agency of Canada, 1015 Arlington St, Winnipeg, MB R3E 3P6, Canada.

Abstract

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 M. tuberculosis infection.

MeSH

Diabetes Mellitus, Comorbidity, Silicosis, Latent Tuberculosis, Lupus Erythematosus, Systemic, Tuberculosis, Viruses, Interferon Type I, Infections