ArticleThe Journal of pathology2014
The IL-13/IL-4Rα axis is involved in tuberculosis-associated pathology.
Article in The Journal of pathology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 87 papers, 1 of them a synthesis that pooled it.
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Who cites it
87 citing papers in PubMed, 1 synthesis or guideline pooled it, 126 citations in OpenAlex.
- Pathology of TB/COVID-19 Co-Infection: The phantom menace.Tuberculosis (Edinburgh, Scotland) · 2021Pooled it
- Trial
- Asthma Incidence and Risk Factors in Tuberculosis Survivors: A Longitudinal Analysis of National Health Data.Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology · 2026Article
- A Distinct Bronchoalveolar Lavage Cytokine Signature Characterizes Nontuberculous Mycobacterial Pulmonary Disease.Medical sciences (Basel, Switzerland) · 2026Article
- Th2 bias and T-cell exhaustion characterize the immunopathology of non-tuberculous mycobacterial pulmonary disease.NPJ systems biology and applications · 2026Article
- CCR6 is essential for effective immunity againstInfection and immunity · 2026Article
- Mouse models of tuberculosis uniformly featuring hypoxic necrotic lesions and poor response to chemotherapy.Infection and immunity · 2026Article
- Sex as a Biological Variable in Tuberculosis Pathogenesis.Immunological reviews · 2026Review
- Mouse Models Uniformly Featuring Human-like Lesions Harboring Drug-tolerantbioRxiv : the preprint server for biology · 2025Article
- Enhanced immunogenicity in mouse by recombinant BCG prime and protein boost based on latency antigen Rv1733c and/or reactivation antigen RpfE.BMC infectious diseases · 2025Article
- Dysplastic lung repair fosters a tuberculosis-promoting microenvironment through maladaptive macrophage polarization.PLoS pathogens · 2025Article
- Aberrant macrophage activation and maladaptive lung repair promote tuberculosis progression uniquely in the lung.bioRxiv : the preprint server for biology · 2025Article
- Arginine metabolism in myeloid cells in health and disease.Seminars in immunopathology · 2025Review
- Fitness costs of Mycobacterium tuberculosis resistant to rifampicin is compensated by rapid Th2 polarization mediated by early and high IL-4 production during mice infection.Scientific reports · 2025Article
- The clinical-stage drug BTZ-043 accumulates in murine tuberculosis lesions and efficiently acts against Mycobacterium tuberculosis.Nature communications · 2025Article
- Case Report: Rare Dupilumab-Associated Pulmonary and Extrapulmonary Tuberculosis.Infection and drug resistance · 2025Article
- Pathogenesis of Post-Tuberculosis Lung Disease: Defining Knowledge Gaps and Research Priorities at the Second International Post-Tuberculosis Symposium.American journal of respiratory and critical care medicine · 2024Review
- Investigating the treatment shortening potential of a combination of bedaquiline, delamanid and moxifloxacin with and without sutezolid, in a murine tuberculosis model with confirmed drug exposures.The Journal of antimicrobial chemotherapy · 2024Article
- Imaging the Architecture of Granulomas Induced by Mycobacterium tuberculosis Infection with Single-molecule Fluorescence In Situ Hybridization.Journal of immunology (Baltimore, Md. : 1950) · 2024Article
- Reappraising the Role of T Cell-Derived IFN-γ in Restriction of Mycobacterium tuberculosis in the Murine Lung.Journal of immunology (Baltimore, Md. : 1950) · 2024Article
27 more citing papers are in PubMed but not listed here.
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Authors and funding
9 authors at 4 institutions in 4 countries.
Funding
Abstract
Human tuberculosis (TB) is a leading global health threat and still constitutes a major medical challenge. However, mechanisms governing tissue pathology during post-primary TB remain elusive, partly because genetically or immunologically tractable animal models are lacking. In human TB, the demonstration of a large relative increase in interleukin (IL)-4 and IL-13 expression, which correlates with lung damage, indicates that a subversive T helper (TH)2 component in the response to Mycobacterium tuberculosis (Mtb) may undermine protective immunity and contribute to reactivation and tissue pathology. Up to now, there has been no clear evidence regarding whether IL-4/IL-13-IL-4 receptor-α (Rα)-mediated mechanisms may in fact cause reactivation and pathology. Unfortunately, the virtual absence of centrally necrotizing granulomas in experimental murine TB is associated with a poor induction of a TH2 immune response. We therefore hypothesize that, in mice, an increased production of IL-13 may lead to a pathology similar to human post-primary TB. In our study, aerosol Mtb infection of IL-13-over-expressing mice in fact resulted in pulmonary centrally necrotizing granulomas with multinucleated giant cells, a hypoxic rim and a perinecrotic collagen capsule, with an adjacent zone of lipid-rich, acid-fast bacilli-containing foamy macrophages, thus strongly resembling the pathology in human post-primary TB. Granuloma necrosis (GN) in Mtb-infected IL-13-over-expressing mice was associated with the induction of arginase-1-expressing macrophages. Indirect blockade of the endogenous arginase inhibitor l-hydroxyarginine in Mtb-infected wild-type mice resulted in a strong arginase expression and precipitated a similar pathology of GN. Together, we here introduce an experimental TB model that displays many features of centrally necrotizing granulomas in human post-primary TB and demonstrate that IL-13/IL-4Rα-dependent mechanisms leading to arginase-1 expression are involved in TB-associated tissue pathology.
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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.