Article in Nature communications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
2 · The registry
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Amirhossein DavariGraduate Program in Pharmaceutical Sciences, College of Graduate Health Sciences, University of Tennessee Health Science Center, Memphis, TN, USA.ORCID http://orcid.org/0000-0002-7492-9299
Brian M PetersDepartment of Clinical Pharmacy and Translational Science, College of Pharmacy, University of Tennessee Health Science Center, Memphis, TN, USA.ORCID http://orcid.org/0000-0002-0445-2077
Michail S LionakisFungal Pathogenesis Section, Laboratory of Clinical Immunology and Microbiology (LCIM), National Institute of Allergy and Infectious Diseases (NIAID), Bethesda, MD, USA.ORCID http://orcid.org/0000-0003-4994-9500
Systems Epigenomics of Persistent Bloodstream InfectionU19AI172713 · NIAID · LUNDQUIST INSTITUTE FOR BIOMEDICAL INNOVATION AT HARBOR-UCLA MEDICAL CENTER · PI ELAINE F REED · 2023 to 2026
$11.6M
Host and Fungal Regulation of Type 17 Immunity to Oral CandidiasisR37DE022550 · NIDCR · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI Sarah L Gaffen · 2017 to 2026
$5.6M
Candidalysin: a key mediator of Candida vaginitis immunopathologyR01AI134796 · NIAID · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI Brian M Peters · 2018 to 2026
$2.9M
Oral commensal fungi and structural immunityR01DE031382 · NIDCR · LUNDQUIST INSTITUTE FOR BIOMEDICAL INNOVATION AT HARBOR-UCLA MEDICAL CENTER · PI Marc Swidergall · 2022 to 2026
$2.5M
Regulation of Candida albicans Pathogenesis by Protein Kinase and Transcription Factor NetworksR01AI177254 · NIAID · UNIVERSITY OF IOWA · PI Scott G Filler, Damian J Krysan · 2024 to 2026
$2.3M
IL-17 Receptor Signaling in the Oral MucosaR01DE022550 · NIDCR · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI GAFFEN, SARAH L · 2012 to 2016
$2.1M
Mouse model of neonatal fungal colonization to study homeostasis and diseaseR21AI187999 · NIAID · LUNDQUIST INSTITUTE FOR BIOMEDICAL INNOVATION AT HARBOR-UCLA MEDICAL CENTER · PI Marc Swidergall · 2025 to 2026
$450k
Unraveling transcriptomic and functional changes to immune sensing neuronal ganglia in response to allergy and bacteriaR21AI159221 · NIAID · LUNDQUIST INSTITUTE FOR BIOMEDICAL INNOVATION AT HARBOR-UCLA MEDICAL CENTER · PI JENDZJOWSKY, NICHOLAS · 2022 to 2023
$438k
Asthmatic inflammation requires neuronal upregulation of B-cellsR56AI175328 · NIAID · LUNDQUIST INSTITUTE FOR BIOMEDICAL INNOVATION AT HARBOR-UCLA MEDICAL CENTER · PI JENDZJOWSKY, NICHOLAS · 2024 to 2024
$332k
California Institute for Regenerative Medicine (CIRM) EDUC4-12837NIAID NIH HHS R01 AI134796NIAID NIH HHS R21 AI187999NIAID NIH HHS U19 AI172713NIDCR NIH HHS R01 DE022550NIDCR NIH HHS R01 DE031382NIDCR NIH HHS R37 DE022550U.S. Department of Health & Human Services | NIH | National Institute of Allergy and Infectious Diseases (NIAID) R01AI177254U.S. Department of Health & Human Services | NIH | National Institute of Allergy and Infectious Diseases (NIAID) R21AI159221U.S. Department of Health & Human Services | NIH | National Institute of Allergy and Infectious Diseases (NIAID) R21AI187999; U19AI172713U.S. Department of Health & Human Services | NIH | National Institute of Allergy and Infectious Diseases (NIAID) R56AI175328U.S. Department of Health & Human Services | NIH | National Institute of Dental and Craniofacial Research (NIDCR) R01DE031382U.S. Department of Health & Human Services | NIH | National Institute of Dental and Craniofacial Research (NIDCR) R37DE022550
6 · The paper itself
Abstract
Mucosal barrier integrity is vital for homeostasis with commensal organisms while preventing pathogen invasion. Here we show that fungal-induced immunosurveillance enhances resistance to fungal outgrowth and tissue invasion by remodeling the oral mucosal epithelial barrier in mouse models of adult and neonatal Candida albicans colonization. Epithelial subset expansion and tissue remodeling are dependent on interleukin-22 and signal transducer and activator of transcription 3 signaling, through a non-canonical receptor complex composed of glycoprotein 130 coupled with the interleukin-22 receptor subunit alpha-1 and the interleukin-10 receptor subunit beta. Epithelial proliferation enhanced antifungal host defenses through the upregulation of antimicrobial peptide expression. Immunosurveillance-induced epithelial remodeling is restricted to the oral mucosa, whereas barrier architecture is reset once fungal-specific immunity developed. Collectively, these findings identify fungal-induced transient mucosal remodeling as a critical determinant of resistance to mucosal fungal infection during early stages of microbial colonization.
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.
Non-canonical IL‑22 receptor signaling remodels the oral mucosal barrier during Candida albicans immunosurveillance. · full record | OpenQuestion