ArticlePloS one2015
Cryptococcus neoformans Infection in Mice Lacking Type I Interferon Signaling Leads to Increased Fungal Clearance and IL-4-Dependent Mucin Production in the Lungs.
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 20 papers.
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Who cites it
20 citing papers in PubMed, 33 citations in OpenAlex.
- The host transcriptional response to real-world cryptococcosis in the setting of advanced HIV disease defines dysregulated immune responses that underlie increased vulnerability to infection.The Journal of infectious diseases · 2026Article
- Pulmonary granuloma formation during latentmBio · 2025Article
- Article
- Inbred Mouse Models inJournal of fungi (Basel, Switzerland) · 2024Review
- The emerging links between immunosenescence in innate immune system and neurocryptococcosis.Frontiers in immunology · 2024Review
- Characteristics of mucin hypersecretion in different inflammatory patterns based on endotypes of chronic rhinosinusitis.Clinical and translational allergy · 2024Review
- Cytomegalovirus viremia and advanced HIV disease: is there an argument for anti-CMV treatment?Expert review of anti-infective therapy · 2023Review
- Mouse Model of Latent Cryptococcal Infection and Reactivation.Methods in molecular biology (Clifton, N.J.) · 2023Article
- Deficiency of lung-specific claudin-18 leads to aggravated infection with Cryptococcus deneoformans through dysregulation of the microenvironment in lungs.Scientific reports · 2021Article
- MDA5 Is an Essential Sensor of a Pathogen-Associated Molecular Pattern Associated with Vitality That Is Necessary for Host Resistance againstJournal of immunology (Baltimore, Md. : 1950) · 2020Article
- Type I Interferons Ameliorate Zinc Intoxication of Candida glabrata by Macrophages and Promote Fungal Immune Evasion.iScience · 2020Article
- Viral infection triggers interferon-induced expulsion of live Cryptococcus neoformans by macrophages.PLoS pathogens · 2020Article
- Article
- Pathogenic Fungal Infection in the Lung.Frontiers in immunology · 2019Review
- Extent of Lung Involvement and Serum Cryptococcal Antigen Test in Non-Human Immunodeficiency Virus Adult Patients with Pulmonary Cryptococcosis.Chinese medical journal · 2018Article
- Corticosteroid suppression of antiviral immunity increases bacterial loads and mucus production in COPD exacerbations.Nature communications · 2018Article
- IL-4-induced caveolin-1-containing lipid rafts aggregation contributes to MUC5AC synthesis in bronchial epithelial cells.Respiratory research · 2017Article
- Article
- Influenza A Virus as a Predisposing Factor for Cryptococcosis.Frontiers in cellular and infection microbiology · 2017Article
- Type I Interferons as Regulators of Lung Inflammation.Frontiers in immunology · 2017Review
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Type I interferons (IFNs) are secreted by many cell types upon stimulation via pattern recognition receptors and bind to IFN-α/β receptor (IFNAR), which is composed of IFNAR1 and IFNAR2. Although type I IFNs are well known as anti-viral cytokines, limited information is available on their role during fungal infection. In the present study, we addressed this issue by examining the effect of IFNAR1 defects on the host defense response to Cryptococcus neoformans. In IFNAR1KO mice, the number of live colonies was lower and the host immune response mediated not only by Th1 but also by Th2 and Th17-related cytokines was more accelerated in the infected lungs than in WT mice. In addition, mucin production by bronchoepithelial cells and expression of MUC5AC, a major core protein of mucin in the lungs, were significantly higher in IFNAR1KO mice than in WT mice. This increase in mucin and MUC5AC production was significantly inhibited by treatment with neutralizing anti-IL-4 mAb. In contrast, administration of recombinant IFN-αA/D significantly suppressed the production of IL-4, but not of IFN-γ and IL-17A, in the lungs of WT mice after cryptococcal infection. These results indicate that defects of IFNAR1 led to improved clearance of infection with C. neoformans and enhanced synthesis of IFN-γ and the IL-4-dependent production of mucin. They also suggest that type I IFNs may be involved in the negative regulation of early host defense to this infection.
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