ArticleFrontiers in cellular and infection microbiology2021
Natural Killer Cells Regulate Pulmonary Macrophages Polarization in Host Defense Against Chlamydial Respiratory Infection.
Article in Frontiers in cellular and infection microbiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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Who cites it
10 citing papers in PubMed, 18 citations in OpenAlex.
- NK Cells: A Powerful Squad Versus SARS-CoV-2.International journal of molecular sciences · 2025Review
- The Importance of Lung Innate Immunity During Health and Disease.Pathogens (Basel, Switzerland) · 2025Review
- Ephedrine attenuates LPS-induced M1 polarization of alveolar macrophages via the PKM2-mediated glycolysis.Toxicology research · 2024Article
- Review
- Lack of the IFN-γ signal leads to lethal Orientia tsutsugamushi infection in mice with skin eschar lesions.PLoS pathogens · 2024Article
- Enhancement of Macrophage Immunity against Chlamydial Infection by Natural Killer T Cells.Cells · 2024Article
- Article
- Regulation of chlamydial colonization by IFNγ delivered via distinct cells.Trends in microbiology · 2023Review
- A Pathogenic Role for FcγRI in the Immune Response against Chlamydial Respiratory Infection.Microorganisms · 2022Article
- Cross Talk Between Natural Killer T and Dendritic Cells and Its Impact on T Cell Responses in Infections.Frontiers in immunology · 2022Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
NK cells and pulmonary macrophages both are important components of innate immunity. The interaction between NK cells and pulmonary macrophages during chlamydial infection is poorly understood. In this study, we explored the effect of NK cells on regulation of pulmonary macrophage function during chlamydial respiratory infection. We found that NK depletion led to polarization of pulmonary macrophages from M1 to M2 phenotype, and it is related to reduced miR-155 expression in lung macrophage. Using adoptive transfer approach, we found that the recipients receiving lung macrophages isolated from
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Registered trials
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