ArticlePloS one2015
IL-4Rα-dependent alternative activation of macrophages is not decisive for Mycobacterium tuberculosis pathology and bacterial burden in mice.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 28 citations in OpenAlex.
- A Rapid Active-Latent-Relapse Murine Model of Tuberculosis Based Blood Transcriptional Signature That Distinguishes Disease Stages.International journal of molecular sciences · 2026Article
- The divergent outcome of IL-4Rα signalling on Foxp3 T regulatory cells in listeriosis and tuberculosis.Frontiers in immunology · 2024Article
- Turning foes into permissive hosts: manipulation of macrophage polarization by intracellular bacteria.Current opinion in immunology · 2023Review
- Host-Directed Targeting of LincRNA-MIR99AHG Suppresses Intracellular Growth ofNucleic acid therapeutics · 2022Article
- Intranasally administered S-MGB-364 displays antitubercular activity and modulates the host immune response to Mycobacterium tuberculosis infection.The Journal of antimicrobial chemotherapy · 2022Article
- Lyl1-deficiency promotes inflammatory responses and increases mycobacterial burden in response toFrontiers in immunology · 2022Article
- In the Thick of It: Formation of the Tuberculous Granuloma and Its Effects on Host and Therapeutic Responses.Frontiers in immunology · 2022Review
- IL-4i1 Regulation of Immune Protection During Mycobacterium tuberculosis Infection.The Journal of infectious diseases · 2021Article
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- IL-4-Responsive B Cells Are Detrimental During Chronic Tuberculosis Infection in Mice.Frontiers in immunology · 2021Article
- Prokaryotic Expression, In Vitro Biological Analysis, and In Silico Structural Evaluation of Guinea Pig IL-4.Molecular biotechnology · 2020Article
- Mycobacterium tuberculosis clinical isolates of the Beijing and East-African Indian lineage induce fundamentally different host responses in mice compared to H37Rv.Scientific reports · 2019Article
- Functional aspects, phenotypic heterogeneity, and tissue immune response of macrophages in infectious diseases.Infection and drug resistance · 2019Article
- Differential Targeting of c-Maf, Bach-1, and Elmo-1 by microRNA-143 and microRNA-365 Promotes the Intracellular Growth ofFrontiers in immunology · 2019Article
- Protein kinase C-delta (PKCδ), a marker of inflammation and tuberculosis disease progression in humans, is important for optimal macrophage killing effector functions and survival in mice.Mucosal immunology · 2018Article
- Genome-wide profiling of transcribed enhancers during macrophage activation.Epigenetics & chromatin · 2017Article
- Immunometabolism within the tuberculosis granuloma: amino acids, hypoxia, and cellular respiration.Seminars in immunopathology · 2016Review
- A Mutation in IL4RA Is Associated with the Degree of Pathology in Human TB Patients.Mediators of inflammation · 2016Article
- Targeting Batf2 for infectious diseases and cancer.Oncotarget · 2015Article
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Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
Abstract
Classical activation of macrophages (caMph or M1) is crucial for host protection against Mycobacterium tuberculosis (Mtb) infection. Evidence suggests that IL-4/IL-13 alternatively activated macrophages (aaMph or M2) are exploited by Mtb to divert microbicidal functions of caMph. To define the functions of M2 macrophages during tuberculosis (TB), we infected mice deficient for IL-4 receptor α on macrophages (LysMcreIL-4Rα-/lox) with Mtb. We show that absence of IL-4Rα on macrophages does not play a major role during infection with Mtb H37Rv, or the clinical Beijing strain HN878. This was demonstrated by similar mortality, bacterial burden, histopathology and T cell proliferation between infected wild-type (WT) and LysMcreIL-4Rα-/lox mice. Interestingly, we observed no differences in the lung expression of inducible nitric oxide synthase (iNOS) and Arginase 1 (Arg1), well-established markers for M1/M2 macrophages among the Mtb-infected groups. Kinetic expression studies of IL-4/IL-13 activated bone marrow-derived macrophages (BMDM) infected with HN878, followed by gene set enrichment analysis, revealed that the MyD88 and IL-6, IL-10, G-CSF pathways are significantly enriched, but not the IL-4Rα driven pathway. Together, these results suggest that IL-4Rα-macrophages do not play a central role in TB disease progression.
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