2025/04/26 by Mark C. Fernandez, Glenna J. Peterson, Chinh T. Lé +2 · 1 voice
Immunology and Microbiology · Medicine · #Immune Cell Function and Interaction #Tuberculosis Research and Epidemiology
paper · doi:10.1093/infdis/jiaf220
openalex created_date 2025/04/26 · openalex publication_date 2025/04/26 · openalex updated_date 2026/06/23
We examined whether interferon-γ (IFNG) restricts Mycobacterium tuberculosis growth in human macrophages across a range of conditions and methods. We observed an IFNG-dependent enhancement of bacterial replication in macrophage colony-stimulating factor-differentiated monocyte-derived macrophages (4.84 × 105 colony-forming units [CFU] IFNG stimulated vs 2.48 × 105 CFU untreated, P < .001) with 4 M. tuberculosis strains. M. tuberculosis replication was not restricted by IFNG treatment of alveolar macrophages. In agreement with previous studies, IFNG-stimulated murine bone marrow-derived macrophages effectively restricted M. tuberculosis replication. These data suggest that M. tuberculosis resists IFNG-stimulated immunity within human macrophages with implications for distinct host species immune responses.