ArticleJournal of immunology (Baltimore, Md. : 1950)2024
Reappraising the Role of T Cell-Derived IFN-γ in Restriction of Mycobacterium tuberculosis in the Murine Lung.
Article in Journal of immunology (Baltimore, Md. : 1950), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed.
- Strong, sustained type I IFN signaling acts cell intrinsically to impair IFNγ responses and cause tuberculosis susceptibility.Cell host & microbe · 2026Article
- Monocytic niches escape T cell surveillance and promote Mycobacterium tuberculosis persistence in lymph nodes.Immunity · 2026Article
- Impaired IFNγ responsiveness of monocyte-derived lung cells limits immunity to Mycobacterium tuberculosis.Nature communications · 2026Article
- HowVaccines · 2026Review
- Strong sustained type I IFN signaling acts cell intrinsically to impair IFNγ responses and cause tuberculosis susceptibility.bioRxiv : the preprint server for biology · 2026Article
- Exploring Host-driven Immunopathological Factors Developing Severe Tuberculosis: Insights from Comparative Mouse Models.International journal of biological sciences · 2026Article
- Helminth Infection, Gut Microbiome Alterations, and Their Impact on Pulmonary Tuberculosis Susceptibility.Journal of tropical medicine · 2026Review
- A quadral biosignature of IFN-γ, IL-2, IL-12 and IP-10 increases the diagnostic potential for latent tuberculosis among diabetic patients in Uganda.BMC immunology · 2025Article
- Impaired IFNγ responsiveness of monocyte-derived lung cells limits immunity tobioRxiv : the preprint server for biology · 2025Article
- Metabolic dysfunction impairs Mycobacterium tuberculosis-specific cytokine and chemokine responses in latent tuberculosis and type 2 diabetes mellitus.Scientific reports · 2025Article
- Macrophage-T cell interactions promote SLAMF1 expression for enhanced TB defense.Nature communications · 2025Article
- Antigen-specific CD4+ T cells promote monocyte recruitment and differentiation into glycolytic lung macrophages to control Mycobacterium tuberculosis.PLoS pathogens · 2025Article
- Increased long-term central memory T cells in patients with retreatment pulmonary tuberculosis.Frontiers in immunology · 2025Article
Corrections and comments
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5 authors.
Funding
Abstract
T cells producing IFN-γ have long been considered a stalwart for immune protection against Mycobacterium tuberculosis (Mtb), but their relative importance to pulmonary immunity has been challenged by murine studies that achieved protection by adoptively transferred Mtb-specific IFN-γ-/- T cells. Using IFN-γ-/- T cell chimeric mice and adoptive transfer of IFN-γ-/- T cells into TCRβ-/-δ-/- mice, we demonstrate that control of lung Mtb burden is in fact dependent on T cell-derived IFN-γ, and, furthermore, mice selectively deficient in T cell-derived IFN-γ develop exacerbated disease compared with T cell-deficient control animals, despite equivalent lung bacterial burdens. Deficiency in T cell-derived IFN-γ skews infected and bystander monocyte-derived macrophages to an alternative M2 phenotype and promotes neutrophil and eosinophil influx. Our studies support an important role for T cell-derived IFN-γ in pulmonary immunity against tuberculosis.
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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 Socratic graph.