ArticleProceedings of the National Academy of Sciences of the United States of America2015
Human IL-32 expression protects mice against a hypervirulent strain of Mycobacterium tuberculosis.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 53 citations in OpenAlex.
- Identifying Single-Cell Expression Quantitative Trait Loci Using a Bootstrap Penalized Hurdle Model.Genes · 2026Article
- Diagnostic accuracy of interleukin 32γ for tuberculous pleural effusion.Journal of thoracic disease · 2025Article
- Cytoadhesion of Plasmodium falciparum-Infected Red Blood Cells Changes the Expression of Cytokine-, Histone- and Antiviral Protein-Encoding Genes in Brain Endothelial Cells.Molecular microbiology · 2024Article
- The Role of mRNA Alternative Splicing in Macrophages Infected withMolecules (Basel, Switzerland) · 2024Review
- Understanding the development of tuberculous granulomas: insights into host protection and pathogenesis, a review in humans and animals.Frontiers in immunology · 2024Review
- The regulation and potential role of interleukin-32 in tuberculous pleural effusion.Frontiers in immunology · 2024Article
- A nod to the bond between NOD2 and mycobacteria.PLoS pathogens · 2023Review
- Article
- Interleukin 32 as a Potential Marker for Diagnosis of Tuberculous Pleural Effusion.Microbiology spectrum · 2022Article
- Interleukin-32Journal of immunology research · 2022Article
- A Critical Overview of Interleukin 32 in Leishmaniases.Frontiers in immunology · 2022Review
- The Research Progress in Immunotherapy of Tuberculosis.Frontiers in cellular and infection microbiology · 2021Review
- Genetic variation in Interleukin-32 influence the immune response against New World Leishmania species and susceptibility to American Tegumentary Leishmaniasis.PLoS neglected tropical diseases · 2020Article
- Differential Responses by Human Macrophages to Infection WithFrontiers in microbiology · 2020Article
- IL-32 and its splice variants are associated with protection against Mycobacterium tuberculosis infection and skewing of Th1/Th17 cytokines.Journal of leukocyte biology · 2020Article
- Article
- The proinflammatory cytokine TNFα induces DNA demethylation-dependent and -independent activation ofThe Journal of biological chemistry · 2019Article
- Interleukin 32 expression in human melanoma.Journal of translational medicine · 2019Article
- Levels of vitamin D-associated cytokines distinguish between active and latent tuberculosis following a tuberculosis outbreak.BMC infectious diseases · 2019Article
- Alpha-1-Antitrypsin Enhances Primary Human Macrophage Immunity Against Non-tuberculous Mycobacteria.Frontiers in immunology · 2019Article
Corrections and comments
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Authors and funding
21 authors at 7 institutions in 3 countries.
Funding
Abstract
Silencing of interleukin-32 (IL-32) in a differentiated human promonocytic cell line impairs killing of Mycobacterium tuberculosis (MTB) but the role of IL-32 in vivo against MTB remains unknown. To study the effects of IL-32 in vivo, a transgenic mouse was generated in which the human IL-32γ gene is expressed using the surfactant protein C promoter (SPC-IL-32γTg). Wild-type and SPC-IL-32γTg mice were infected with a low-dose aerosol of a hypervirulent strain of MTB (W-Beijing HN878). At 30 and 60 d after infection, the transgenic mice had 66% and 85% fewer MTB in the lungs and 49% and 68% fewer MTB in the spleens, respectively; the transgenic mice also exhibited greater survival. Increased numbers of host-protective innate and adaptive immune cells were present in SPC-IL-32γTg mice, including tumor necrosis factor-alpha (TNFα) positive lung macrophages and dendritic cells, and IFN-gamma (IFNγ) and TNFα positive CD4(+) and CD8(+) T cells in the lungs and mediastinal lymph nodes. Alveolar macrophages from transgenic mice infected with MTB ex vivo had reduced bacterial burden and increased colocalization of green fluorescent protein-labeled MTB with lysosomes. Furthermore, mouse macrophages made to express IL-32γ but not the splice variant IL-32β were better able to limit MTB growth than macrophages capable of producing both. The lungs of patients with tuberculosis showed increased IL-32 expression, particularly in macrophages of granulomas and airway epithelial cells but also B cells and T cells. We conclude that IL-32γ enhances host immunity to MTB.
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