ArticlePLoS neglected tropical diseases2019
The cell fate regulator NUPR1 is induced by Mycobacterium leprae via type I interferon in human leprosy.
Article in PLoS neglected tropical diseases, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.
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Who cites it
9 citing papers in PubMed, 1 synthesis or guideline pooled it, 15 citations in OpenAlex.
- An update on leprosy immunopathogenesis: systematic review.Frontiers in immunology · 2024Pooled it
- Locat: Joint enrichment and depletion testing identifies localized marker genes in single-cell transcriptomics.bioRxiv : the preprint server for biology · 2026Article
- Dynamics of Th1/Th17 responses and antimicrobial pathways in leprosy skin lesions.The Journal of clinical investigation · 2025Article
- Inflammatory Gene Signature Identified by Machine Algorithms Reveals Novel Biomarkers of Coronary Artery Disease.Journal of inflammation research · 2025Article
- Article
- Xenophagy as a Strategy forPathogens (Basel, Switzerland) · 2023Review
- Gene Expression Profile ofFrontiers in medicine · 2022Article
- Human macrophage polarization in the response toCurrent research in microbial sciences · 2021Article
- Blood RNA signature RISK4LEP predicts leprosy years before clinical onset.EBioMedicine · 2021Article
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Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
Abstract
The initial interaction between a microbial pathogen and the host immune response influences the outcome of the battle between the host and the foreign invader. Leprosy, caused by the obligate intracellular pathogen Mycobacterium leprae, provides a model to study relevant human immune responses. Previous studies have adopted a targeted approach to investigate host response to M. leprae infection, focusing on the induction of specific molecules and pathways. By measuring the host transcriptome triggered by M. leprae infection of human macrophages, we were able to detect a host gene signature 24-48 hours after infection characterized by specific innate immune pathways involving the cell fate mechanisms autophagy and apoptosis. The top upstream regulator in the M. leprae-induced gene signature was NUPR1, which is found in the M. leprae-induced cell fate pathways. The induction of NUPR1 by M. leprae was dependent on the production of the type I interferon (IFN), IFN-β. Furthermore, NUPR1 mRNA and protein were upregulated in the skin lesions from patients with the multibacillary form of leprosy. Together, these data indicate that M. leprae induces a cell fate program which includes NUPR1 as part of the host response in the progressive form of leprosy.
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Registered trials
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