ArticleThe Journal of experimental medicine2011
Regulation of neutrophils by interferon-γ limits lung inflammation during tuberculosis infection.
Article in The Journal of experimental medicine, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 251 papers.
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Who cites it
251 citing papers in PubMed, 369 citations in OpenAlex.
- Airway immune signatures of protection and disease progression in recent human tuberculosis household contacts.Nature immunology · 2026Article
- Neutrophils and tuberculosis - insights into immunobiology and pathogenesis.Molecular biology reports · 2026Review
- IFN𝛾 and IFN𝛾 mimetics prevent IFN-I-mediated TB susceptibility by regulating iron metabolism and lipid peroxidation.bioRxiv : the preprint server for biology · 2026Article
- Plasma TIM-1 concentration: correlation with cytokines in pulmonary tuberculosis patients and development of a predictive model.BMC pulmonary medicine · 2026Article
- CD39 regulates P2RX7-mediated lung necrotic lesions in severe experimental tuberculosis.Mucosal immunology · 2026Article
- The host immune response to Mycobacterium tuberculosis determining protection or disease progression.Nature immunology · 2026Review
- Cas9eLife · 2026Article
- CCR6 is essential for effective immunity againstInfection and immunity · 2026Article
- Context-specific roles for IL-17 in tuberculosis.PLoS pathogens · 2026Review
- Ly6GeLife · 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
- Spatial and temporal immune landscapes of non-necrotic granulomas in two murine tuberculosis models with divergent disease outcomes.Frontiers in immunology · 2026Article
- Second-order regulation: IFN-γ suppresses IL-17A-mediated type 3 inflammation.Frontiers in immunology · 2026Article
- Exploring Host-driven Immunopathological Factors Developing Severe Tuberculosis: Insights from Comparative Mouse Models.International journal of biological sciences · 2026Article
- T cell-macrophage interactions in tuberculosis: What we've got here is failure to communicate.Journal of internal medicine · 2026Review
- Diagnostic value of quantitative SPECT/CT integrated parameters for differentiating spinal tuberculosis from spinal metastases.Frontiers in oncology · 2026Article
- IFN-γ and IL-17 elicit synergistic anti-mycobacterial responses by inhibiting coronin-1A retention.Communications biology · 2025Article
- Type I IFN drives neutrophil swarming, impeding lung T cell-macrophage interactions and TB control.The Journal of experimental medicine · 2025Article
- Review and comprehensive analysis of knowledge, tools, and implementation gaps for the control of contagious bovine pleuropneumonia.BMC veterinary research · 2025Review
- Mycobacterium tuberculosis-specific T cells restrain anti-cancer drug-induced neutrophilic lung inflammation in tuberculosis.Nature communications · 2025Article
191 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
2 authors at 2 institutions in 1 country.
Funding
Abstract
Resistance to Mycobacterium tuberculosis requires the host to restrict bacterial replication while preventing an over-exuberant inflammatory response. Interferon (IFN) γ is crucial for activating macrophages and also regulates tissue inflammation. We dissociate these two functions and show that IFN-γ(-/-) memory CD4(+) T cells retain their antimicrobial activity but are unable to suppress inflammation. IFN-γ inhibits CD4(+) T cell production of IL-17, which regulates neutrophil recruitment. In addition, IFN-γ directly inhibits pathogenic neutrophil accumulation in the infected lung and impairs neutrophil survival. Regulation of neutrophils is important because their accumulation is detrimental to the host. We suggest that neutrophilia during tuberculosis indicates failed Th1 immunity or loss of IFN-γ responsiveness. These results establish an important antiinflammatory role for IFN-γ in host protection against tuberculosis.
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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.