ArticleInfection and immunity2015
STAT1 signaling within macrophages is required for antifungal activity against Cryptococcus neoformans.
Article in Infection and immunity, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
64 citing papers in PubMed, 95 citations in OpenAlex.
- Extracellular Vesicles fromJournal of fungi (Basel, Switzerland) · 2026Article
- Transcriptomic and lipidomic analysis of the cryptococcal lung granuloma reveals macrophage boundary programs and sphingolipid remodeling.Nature communications · 2026Article
- STAT1 expression in myeloid cells restrains murine norovirus-induced hepatitis and fibrosis.bioRxiv : the preprint server for biology · 2026Article
- Immunomodulatory activity of Pleurotus pulmonarius crude extract to human monocyte against Cryptococcus neoformans.BMC complementary medicine and therapies · 2025Article
- Editorial: Exploring the molecular mechanisms that regulate macrophage polarization.Frontiers in immunology · 2025Article
- Clinical characteristics and prognostic factors of pulmonary and extrapulmonary cryptococcosis.BMC infectious diseases · 2024Article
- Article
- S100A9 deletion in microglia/macrophages ameliorates brain injury through the STAT6/PPARγ pathway in ischemic stroke.CNS neuroscience & therapeutics · 2024Article
- Cryptococcosis Associated With Biologic Therapy: A Narrative Review.Open forum infectious diseases · 2024Review
- Inbred Mouse Models inJournal of fungi (Basel, Switzerland) · 2024Review
- The dual role of LOXL4 in the pathogenesis and development of human malignant tumors: a narrative review.Translational cancer research · 2024Review
- Article
- Microglia are not protective against cryptococcal meningitis.Nature communications · 2023Article
- Kicking sleepers out of bed: Macrophages promote reactivation of dormant Cryptococcus neoformans by extracellular vesicle release and non-lytic exocytosis.PLoS pathogens · 2023Article
- Innate Pulmonary Phagocytes and Their Interactions with PathogenicJournal of fungi (Basel, Switzerland) · 2023Review
- Regulation of macrophage IFNγ-stimulated gene expression by the transcriptional coregulator CITED1.Journal of cell science · 2023Article
- Macrophages in periodontitis: A dynamic shift between tissue destruction and repair.The Japanese dental science review · 2022Review
- Macrophage Phenotypes and Gene Expression Patterns Are Unique in Naturally Occurring Metabolically Healthy Obesity.International journal of molecular sciences · 2022Article
- Review
- Review
4 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
6 authors at 3 institutions in 2 countries.
Funding
Abstract
Cryptococcus neoformans, the predominant etiological agent of cryptococcosis, is an opportunistic fungal pathogen that primarily affects AIDS patients and patients undergoing immunosuppressive therapy. In immunocompromised individuals, C. neoformans can lead to life-threatening meningoencephalitis. Studies using a virulent strain of C. neoformans engineered to produce gamma interferon (IFN-γ), denoted H99γ, demonstrated that protection against pulmonary C. neoformans infection is associated with the generation of a T helper 1 (Th1)-type immune response and signal transducer and activator of transcription 1 (STAT1)-mediated classical (M1) macrophage activation. However, the critical mechanism by which M1 macrophages mediate their anti-C. neoformans activity remains unknown. The current studies demonstrate that infection with C. neoformans strain H99γ in mice with macrophage-specific STAT1 ablation resulted in severely increased inflammation of the pulmonary tissue, a dysregulated Th1/Th2-type immune response, increased fungal burden, deficient M1 macrophage activation, and loss of protection. STAT1-deficient macrophages produced significantly less nitric oxide (NO) than STAT1-sufficient macrophages, correlating with an inability to control intracellular cryptococcal proliferation, even in the presence of reactive oxygen species (ROS). Furthermore, macrophages from inducible nitric oxide synthase knockout mice, which had intact ROS production, were deficient in anticryptococcal activity. These data indicate that STAT1 activation within macrophages is required for M1 macrophage activation and anti-C. neoformans activity via the production of NO.
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What OpenQuestion holds
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.