ArticleJCI insight2023
MDA5 RNA-sensing pathway activation by Mycobacterium tuberculosis promotes innate immune subversion and pathogen survival.
Article in JCI insight, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 26 citations in OpenAlex.
- Canonical and noncanonical autophagy in immunity.Immunity · 2026Review
- Loss of cellular RNA homeostasis contributes to MDA5 activation during virus infection.Nature immunology · 2026Article
- Network toxicology and multi-omics identify potential interactions between between air pollutants and interferon-related signaling in tuberculosis.Molecular biology reports · 2026Article
- Dual human lung models reveal compartment-specific activity of anti-tuberculosis drugs and host-directed therapies.Microbiology spectrum · 2026Article
- Identification and optimization of first-in-class RNA helicase inhibitors of DDX1, LGP2, and MDA5.European journal of medicinal chemistry · 2026Article
- The ubiquitin ligase CBL and Fas-associated factor 2 cooperate to regulate the innate immune response to M. tuberculosis.PLoS pathogens · 2026Article
- Molecular signaling in coinfection: howFrontiers in immunology · 2026Review
- Mycobacterium tuberculosis triggers reduced inflammatory cytokine responses and virulence in mice lacking Tax1bp1.PLoS pathogens · 2025Article
- Loss of theScience advances · 2025Article
- The immune system in cardiovascular diseases: from basic mechanisms to therapeutic implications.Signal transduction and targeted therapy · 2025Review
- Identification of immune phenotypes and diagnostic biomarkers in active and latent tuberculosis infections.Scientific reports · 2025Article
- Case report: Exploring efficacy of tofacitinib in modulating interferon response in five case of anti-MDA5+ dermatomyositis with interstitial lung disease.Frontiers in immunology · 2025Article
- Established and Emerging Roles of DEAD/H-Box Helicases in Regulating Infection and Immunity.Immunological reviews · 2025Review
- Article
- Tax1bp1 enhances bacterial virulence and promotes inflammatory responses duringbioRxiv : the preprint server for biology · 2024Article
- The balance between antiviral and antibacterial responses duringbioRxiv : the preprint server for biology · 2024Article
- Endogenous Retroviruses Unveiled: A Comprehensive Review of Inflammatory Signaling/Senescence-Related Pathways and Therapeutic Strategies.Aging and disease · 2024Review
- Roles of Lipolytic enzymes inFrontiers in microbiology · 2024Review
- Mycobacterial Nucleic Acids Modulate Host Innate Immune Responses.Journal of infectious disease and therapy · 2024Article
- An intracellular bacterial pathogen triggers RIG-I/MDA5-dependent necroptosis.Current research in microbial sciences · 2024Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Host cytosolic sensing of Mycobacterium tuberculosis (M. tuberculosis) RNA by the RIG-I-like receptor (RLR) family perturbs innate immune control within macrophages; however, a distinct role of MDA5, a member of the RLR family, in M. tuberculosis pathogenesis has yet to be fully elucidated. To further define the role of MDA5 in M. tuberculosis pathogenesis, we evaluated M. tuberculosis intracellular growth and innate immune responses in WT and Mda5-/- macrophages. Transfection of M. tuberculosis RNA strongly induced proinflammatory cytokine production in WT macrophages, which was abrogated in Mda5-/- macrophages. M. tuberculosis infection in macrophages induced MDA5 protein expression, accompanied by an increase in MDA5 activation as assessed by multimer formation. IFN-γ-primed Mda5-/- macrophages effectively contained intracellular M. tuberculosis proliferation to a markedly greater degree than WT macrophages. Further comparisons of WT versus Mda5-/- macrophages revealed that during M. tuberculosis infection MDA5 contributed to IL-1β production and inflammasome activation and that loss of MDA5 led to a substantial increase in autophagy. In the mouse TB model, loss of MDA5 conferred host survival benefits with a concomitant reduction in M. tuberculosis bacillary burden. These data reveal that loss of MDA5 is host protective during M. tuberculosis infection in vitro and in vivo, suggesting that M. tuberculosis exploits MDA5 to subvert immune containment.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.