ArticleJournal of immunology (Baltimore, Md. : 1950)2013
TPL-2-ERK1/2 signaling promotes host resistance against intracellular bacterial infection by negative regulation of type I IFN production.
Article in Journal of immunology (Baltimore, Md. : 1950), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers.
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Who cites it
71 citing papers in PubMed, 100 citations in OpenAlex.
- PGE2 displays immunosuppressive effects during human active tuberculosis.Scientific reports · 2021Trial
- Strong, sustained type I IFN signaling acts cell intrinsically to impair IFNγ responses and cause tuberculosis susceptibility.Cell host & microbe · 2026Article
- Influenza coinfection inhibits control of mycobacterial infection in a human challenge model.Nature communications · 2026Article
- Strong sustained type I IFN signaling acts cell intrinsically to impair IFNγ responses and cause tuberculosis susceptibility.bioRxiv : the preprint server for biology · 2026Article
- Type I interferon restricts mRNA vaccine efficacy through suppression of antigen uptake in cDCs.NPJ vaccines · 2026Article
- Article
- Pharmacological Stimulator of Interferon Genes Activation Enhances Autophagy-Mediated Clearance of <italic>Mycobacterium tuberculosis</italic> in Human Macrophages.Journal of innate immunity · 2026Article
- Pharmacological inhibition of USP18 improves antibacterial responses and the intracellular control ofFrontiers in immunology · 2026Article
- Mycobacterium tuberculosis triggers reduced inflammatory cytokine responses and virulence in mice lacking Tax1bp1.PLoS pathogens · 2025Article
- Interleukin-1 receptor antagonist is a conserved early factor for exacerbating tuberculosis susceptibility.bioRxiv : the preprint server for biology · 2025Article
- Class IIa histone deacetylase (HDAC) inhibitor TMP269 suppresses lumpy skin disease virus replication by regulating host lysophosphatidic acid metabolism.Journal of virology · 2025Article
- TPL2 kinase activity is required forFrontiers in immunology · 2025Article
- Type I interferons in bacterial diseases: myeloid cells at the crossroads of protection and pathology.Frontiers in immunology · 2025Review
- Increased serum interferon activity in sarcoidosis compared to that in tuberculosis: Implication for diagnosis?Heliyon · 2024Article
- Cytosolic serpins act in a cytoprotective feedback loop that limits ESX-1-dependent death ofmBio · 2024Article
- Type I interferon signaling promotes radioresistance in head and neck cancer.Translational cancer research · 2024Article
- Article
- Host-directed immunotherapy of viral and bacterial infections: past, present and future.Nature reviews. Immunology · 2023Review
- The Influenza-Induced Pulmonary Inflammatory Exudate in Susceptible Tpl2-Deficient Mice Is Dictated by Type I IFN Signaling.Inflammation · 2023Article
- tiRNAs: Insights into Their Biogenesis, Functions, and Future Applications in Livestock Research.Non-coding RNA · 2022Review
11 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 6 institutions in 4 countries.
Funding
Abstract
Tuberculosis, caused by Mycobacterium tuberculosis, remains a leading cause of mortality and morbidity worldwide, causing ≈ 1.4 million deaths per year. Key immune components for host protection during tuberculosis include the cytokines IL-12, IL-1, and TNF-α, as well as IFN-γ and CD4(+) Th1 cells. However, immune factors determining whether individuals control infection or progress to active tuberculosis are incompletely understood. Excess amounts of type I IFN have been linked to exacerbated disease during tuberculosis in mouse models and to active disease in patients, suggesting tight regulation of this family of cytokines is critical to host resistance. In addition, the immunosuppressive cytokine IL-10 is known to inhibit the immune response to M. tuberculosis in murine models through the negative regulation of key proinflammatory cytokines and the subsequent Th1 response. We show in this study, using a combination of transcriptomic analysis, genetics, and pharmacological inhibitors, that the TPL-2-ERK1/2 signaling pathway is important in mediating host resistance to tuberculosis through negative regulation of type I IFN production. The TPL-2-ERK1/2 signaling pathway regulated production by macrophages of several cytokines important in the immune response to M. tuberculosis as well as regulating induction of a large number of additional genes, many in a type I IFN-dependent manner. In the absence of TPL-2 in vivo, excess type I IFN promoted IL-10 production and exacerbated disease. These findings describe an important regulatory mechanism for controlling tuberculosis and reveal mechanisms by which type I IFN may promote susceptibility to this important disease.
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Registered trials
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