ArticleCommunications biology2022
Human M1 macrophages express unique innate immune response genes after mycobacterial infection to defend against tuberculosis.
Article in Communications biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 61 citations in OpenAlex.
- Role of Exosomes During Mycobacterium Tuberculosis Infection: A Double-Edged Sword.Biomedicines · 2026Review
- Tuberculosis and Cellular Metabolism: Insights into the Crosstalk Between Macrophage Immunometabolism and Muscle Dysregulation.International journal of molecular sciences · 2026Review
- Sirtuin2 blockade inhibits replication of human immunodeficiency virus-1 and Mycobacterium tuberculosis in macrophages and humanized mice.Molecular therapy : the journal of the American Society of Gene Therapy · 2026Article
- Mycobacterium tuberculosis-induced PCBP1 degradation drives macrophage ferroptosis to promote infection: a lung-macrophage-targeted RNAa nanotherapy.Journal of nanobiotechnology · 2026Article
- Mycobacterium tuberculosis reinforces M2 polarization of macrophages by activating glutamine metabolism.Brazilian journal of microbiology : [publication of the Brazilian Society for Microbiology] · 2026Article
- Effect of PKM2 onFrontiers in cellular and infection microbiology · 2026Article
- The pathway of autophagy in the epigenetic landscape ofAutophagy · 2025Review
- Immunotherapy for tuberculosis: current strategies and future directions.Military Medical Research · 2025Review
- Cannabinoid Receptor 2 (CB2) in Macrophages: A Promising Clinical Target for Immune Disorders.International journal of molecular sciences · 2025Review
- Long non-coding RNA transcripts inNon-coding RNA research · 2025Review
- Crosstalk between metabolism and epigenetics during macrophage polarization.Epigenetics & chromatin · 2025Review
- Necrosis drives susceptibility toInfection and immunity · 2025Article
- Increased autophagy activity regulated by LC3B gene promoter DNA methylation is associated with progression to active pulmonary tuberculosis disease.Respiratory research · 2025Article
- Prevention of tuberculosis in cynomolgus macaques by an attenuated Mycobacterium tuberculosis vaccine candidate.Nature communications · 2025Article
- Bacterial-Mediated In Situ Engineering of Tumour-Associated Macrophages for Cancer Immunotherapy.Cancers · 2025Review
- Where lung cancer and tuberculosis intersect: recent advances.Frontiers in immunology · 2025Review
- Immunomodulation by bacterial products promotes innate signatures favorable to macrophage responses in tuberculosis infection.Frontiers in immunology · 2025Article
- Dysregulated macrophage immunity inFrontiers in immunology · 2025Review
- Copper homeostasis; A rapier between mycobacteria and macrophages.FASEB bioAdvances · 2025Review
- Therapeutic potential of 7-oxo-DHEA as an adjunctive host-directed therapy for pulmonary tuberculosis.BBA advances · 2025Article
Corrections and comments
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Authors and funding
22 authors at 10 institutions in 3 countries.
Funding
Abstract
Mycobacterium tuberculosis (Mtb) is responsible for approximately 1.5 million deaths each year. Though 10% of patients develop tuberculosis (TB) after infection, 90% of these infections are latent. Further, mice are nearly uniformly susceptible to Mtb but their M1-polarized macrophages (M1-MΦs) can inhibit Mtb in vitro, suggesting that M1-MΦs may be able to regulate anti-TB immunity. We sought to determine whether human MΦ heterogeneity contributes to TB immunity. Here we show that IFN-γ-programmed M1-MΦs degrade Mtb through increased expression of innate immunity regulatory genes (Inregs). In contrast, IL-4-programmed M2-polarized MΦs (M2-MΦs) are permissive for Mtb proliferation and exhibit reduced Inregs expression. M1-MΦs and M2-MΦs express pro- and anti-inflammatory cytokine-chemokines, respectively, and M1-MΦs show nitric oxide and autophagy-dependent degradation of Mtb, leading to increased antigen presentation to T cells through an ATG-RAB7-cathepsin pathway. Despite Mtb infection, M1-MΦs show increased histone acetylation at the ATG5 promoter and pro-autophagy phenotypes, while increased histone deacetylases lead to decreased autophagy in M2-MΦs. Finally, Mtb-infected neonatal macaques express human Inregs in their lymph nodes and macrophages, suggesting that M1 and M2 phenotypes can mediate immunity to TB in both humans and macaques. We conclude that human MФ subsets show unique patterns of gene expression that enable differential control of TB after infection. These genes could serve as targets for diagnosis and immunotherapy of TB.
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