ArticleImmune network2010
Fcgamma receptors modulate pulmonary inflammation by activating innate immune cells in murine hypersensitivity pneumonitis.
Article in Immune network, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed, 3 citations in OpenAlex.
- How experimental models have unlocked hidden mechanisms of hypersensitivity pneumonitis.European respiratory review : an official journal of the European Respiratory Society · 2026Review
- Dietary supplementation ofFrontiers in nutrition · 2023Article
- Immunotherapy in allergy and cellular tests: state of art.Human vaccines & immunotherapeutics · 2014Review
- Management of hypersensivity pneumonitis.Clinical and translational allergy · 2013Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundHypersensitivity pneumonitis (HP) is an interstitial lung disease that develops following repeated exposure to inhaled particulate antigens. The family of Fcgamma receptors (FcgammaRs) has emerged as central regulators for modulating both pro-and anti-inflammatory responses. However, the role of FcgammaRs in the development of HP has not been investigated yet.
methodsTo explore the functional roles of FcgammaRs in HP, FcgammaR(-/-) and B6 mice were challenged with Saccharopolyspora rectivirgula (SR) antigen intranasally, and compared these mice in terms of the histological change, infiltrated immune cells in BALF and in vitro immune responses.
resultsFcgammaR(-/-) mice exhibited attenuation of HP in terms of histological alterations, and reduced numbers of neutrophils and macrophages in and the increased CD4:CD8 ratio of bronchoalveolar lavage fluid. The lungs of FcgammaR(-/-) mice showed high production of Th2 cytokine such as IL-4 and slightly low production of Th1 cytokine, INF-gamma compared to those of B6 mice. However, SR-specific adaptive immune responses of FcgammaR(-/-) mice were similar to those of B6 mice.
conclusionThese results demonstrate that activating Fcgamma receptors play an important role in activating neutrophils and macrophages in pulmonary inflammation and inducing Th1 differentiation by regulating cytokine expression in SR-induced HP.
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Registered trials
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