ArticleJournal of immunology (Baltimore, Md. : 1950)2014
Role of neutrophils in IL-17-dependent immunity to mucosal candidiasis.
Article in Journal of immunology (Baltimore, Md. : 1950), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 87 papers.
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.
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.
Who cites it
87 citing papers in PubMed, 123 citations in OpenAlex.
- IL-1 family signalling drives mucosal defence against systemic Candida albicans infection.Nature microbiology · 2026Article
- Context-specific roles for IL-17 in tuberculosis.PLoS pathogens · 2026Review
- B cell-intrinsic interleukin 17 receptor A signaling supports the establishment of chronic murine gammaherpesvirus 68 infection.Journal of virology · 2025Article
- Impact of emerging and re-emerging viral infections on periodontitis progression.Archives of microbiology · 2025Review
- Abundant Yet Aberrant T Helper Cell Responses to Candida albicans Underlie Mucosal Candidiasis in Humans and Mice.European journal of immunology · 2025Article
- Neutrophil swarming is crucial for limiting oral mucosal infection by Candida albicans.Journal of leukocyte biology · 2025Article
- Comprehensive Review on Tinea Infection Therapies: Allopathic and Herbal Approaches for Dermatophytosis.Recent advances in anti-infective drug discovery · 2025Review
- The molecular mechanism of traditional Chinese medicine in the treatment of oropharyngeal candidiasis (OPC).Journal of oral microbiology · 2025Review
- From High Protection to Lethal Effect: Diverse Outcomes of Immunization Against Invasive Candidiasis with DifferentInternational journal of molecular sciences · 2024Article
- Lack of TYK2 signaling enhances host resistance to Candida albicans skin infection.Nature communications · 2024Article
- Review
- Gut mycobiome in metabolic diseases: Mechanisms and clinical implication.Biomedical journal · 2024Review
- Neutrophil swarms containing myeloid-derived suppressor cells are crucial for limiting oral mucosal infection by C. albicans.Research square · 2023Article
- The Role of Host and Fungal Factors in the Commensal-to-Pathogen Transition ofCurrent clinical microbiology reports · 2023Review
- Mucosal Infection with Unmasked Candida albicans Cells Impacts Disease Progression in a Host Niche-Specific Manner.Infection and immunity · 2022Article
- Pathogenesis and virulence ofVirulence · 2022Review
- Harnessing the Immune Response to Fungal Pathogens for Vaccine Development.Annual review of microbiology · 2022Review
- Review
- A Fun-Guide to Innate Immune Responses to Fungal Infections.Journal of fungi (Basel, Switzerland) · 2022Review
- Radiation Exposure Perturbs IL-17RA-Mediated Immunity Leading to Changes in Neutrophil Responses That Increase Susceptibility to Oropharyngeal Candidiasis.Journal of fungi (Basel, Switzerland) · 2022Article
27 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issued
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Oropharyngeal candidiasis (OPC), caused by the commensal fungus Candida albicans, is an opportunistic infection associated with infancy, AIDS, and IL-17-related primary immunodeficiencies. The Th17-associated cytokines IL-23 and IL-17 are crucial for immunity to OPC, but the mechanisms by which they mediate immunity are poorly defined. IL-17RA-deficient humans and mice are strongly susceptible to OPC, with reduced levels of CXC chemokines and concomitantly impaired neutrophil recruitment to the oral mucosa. Paradoxically, humans with isolated neutropenia are typically not susceptible to candidiasis. To determine whether immunity to OPC is mediated via neutrophil recruitment, mice lacking CXCR2 were subjected to OPC and were found to be highly susceptible, although there was no dissemination of fungi to peripheral organs. To assess whether the entire neutrophil response is IL-17 dependent, IL-17RA(-/-) and IL-23(-/-) mice were administered neutrophil-depleting Abs and subjected to OPC. These mice displayed increased oral fungal burdens compared with IL-17RA(-/-) or IL-23(-/-) mice alone, indicating that additional IL-17-independent signals contribute to the neutrophil response. WT mice treated with anti-Gr-1 Abs exhibited a robust infiltrate of CD11b(+)Ly-6G(low)F4/80(-) cells to the oral mucosa but were nonetheless highly susceptible to OPC, indicating that this monocytic influx is insufficient for host defense. Surprisingly, Ly-6G Ab treatment did not induce the same strong susceptibility to OPC in WT mice. Thus, CXCR2(+) and Gr-1(+) neutrophils play a vital role in host defense against OPC. Moreover, defects in the IL-23/17 axis cause a potent but incomplete deficiency in the neutrophil response to oral candidiasis.
Indexed as
Identifiers
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.