ArticleThe Journal of infectious diseases2025
c-Myc Inhibits Macrophage Antimycobacterial Response in Mycobacterium tuberculosis Infection.
Article in The Journal of infectious diseases, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers, 1 of them a synthesis that pooled it.
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Who cites it
3 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Type 2 diabetes mellitus associated microRNAs in tuberculosis susceptibility: a systematic review and bioinformatic analysis.Frontiers in endocrinology · 2026Pooled it
- MYC at the tumor-immune interface: mechanisms of immune escape and immunotherapy resistance.Frontiers in immunology · 2026Review
- Age-related severity of nontuberculous mycobacterial lung disease is mediated by aberrant macrophage responses and lung microbial dysbiosis.The Journal of infection · 2025Article
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Authors and funding
18 authors.
Funding
Abstract
backgroundMycobacterium tuberculosis (MTB) remains a major cause of global mortality, yet natural immunity prevents disease in more than 90% of exposed individuals. Interferon gamma (IFN-γ) is a critical regulator of innate immunity and enhances macrophage antimicrobial responses.
methodsUsing in vitro systems approaches, we compared the effects of IFN-γ exposure before versus after infection. We manipulated c-Myc in primary macrophages with a tetracycline-inducible lentiviral system. c-Myc expression was also analyzed in tissues from murine tuberculosis models and human granulomas.
resultsPreinfection IFN-γ exposure primed macrophages for enhanced bacterial control, whereas postinfection exposure did not. We identified c-Myc signaling as a central determinant of macrophage antimycobacterial function. Inhibition of c-Myc via Omomyc enhanced bacterial control partly through mTORC1-dependent metabolic reprogramming and nitric oxide production. In vivo analyses, including murine models and human clinical histopathology, revealed strong associations between c-Myc expression, MTB persistence, and active tuberculosis.
conclusionc-Myc mediates immune privilege in MTB infection and represents a promising target for host-directed therapies to enhance macrophage function.
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