ArticleInfection and immunity2011
Regulation of innate immune response to Candida albicans infections by αMβ2-Pra1p interaction.
Article in Infection and immunity, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 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
55 citing papers in PubMed, 78 citations in OpenAlex.
- Clinical evaluation of Candida albicans enolase 1 as a novel biomarker for vulvovaginal candidiasis: a pilot study demonstrating rule-out capability.BMC women's health · 2026Article
- Elevated vaginal heparan sulfate correlates with impaired neutrophil killing ofInfection and immunity · 2026Article
- Inflammatory cytokine signalling in vulvovaginal candidiasis: a hot mess driving immunopathology.Oxford open immunology · 2024Review
- How metals fuel fungal virulence, yet promote anti-fungal immunity.Disease models & mechanisms · 2023Review
- How Gut Bacterial Dysbiosis Can PromoteMicroorganisms · 2022Review
- Influence of Glucose onAntibiotics (Basel, Switzerland) · 2022Article
- Management of recurrent vulvovaginal candidosis: Narrative review of the literature and European expert panel opinion.Frontiers in cellular and infection microbiology · 2022Review
- Methods Related to the Immunopathogenesis of Vulvovaginal Candidiasis and Associated Neutrophil Anergy.Methods in molecular biology (Clifton, N.J.) · 2022Article
- Neutrophil-Specific Knockdown of β2 Integrins Impairs Antifungal Effector Functions and Aggravates the Course of Invasive Pulmonal Aspergillosis.Frontiers in immunology · 2022Article
- The histone chaperone HIR maintains chromatin states to control nitrogen assimilation and fungal virulence.Cell reports · 2021Article
- Insights on the Functional Role of Beta-Glucans in Fungal Immunity Using Receptor-Deficient Mouse Models.International journal of molecular sciences · 2021Review
- Immune Sensing ofJournal of fungi (Basel, Switzerland) · 2021Review
- It Takes Two to Tango: How a Dysregulation of the Innate Immunity, Coupled WithFrontiers in microbiology · 2021Review
- H89 Treatment Reduces Intestinal Inflammation andMicroorganisms · 2020Article
- How Fungal Glycans Modulate Platelet Activation via Toll-Like Receptors Contributing to the Escape ofAntibiotics (Basel, Switzerland) · 2020Review
- Multi trace element profiling in pathogenic and non-pathogenic fungi.Fungal biology · 2020Article
- β2 Integrins-Multi-Functional Leukocyte Receptors in Health and Disease.International journal of molecular sciences · 2020Review
- Review
- How to boost the immune defence prior to respiratory virus infections with the special focus on coronavirus infections.Gut pathogens · 2020Review
- Mechanisms of PathogenicFrontiers in cellular and infection microbiology · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Candida albicans is a common opportunistic fungal pathogen and is the leading cause of invasive fungal diseases in immunocompromised individuals. The induction of cell-mediated immunity to C. albicans is one of the main tasks of cells of the innate immune system, and in vitro evidence suggests that integrin α(M)β₂ (CR3, Mac-1, and CD11b/CD18) is the principal leukocyte receptor involved in recognition of the fungus. Using α(M)β₂-KO mice and mutated strains of C. albicans in two models of murine candidiasis, we demonstrate that neutrophils derived from mice deficient in α(M)β₂ have a reduced ability to kill C. albicans and that the deficient mice themselves exhibit increased susceptibility to fungal infection. Disruption of the PRA1 gene of C. albicans, the primary ligand for α(M)β₂, protects the fungus against leukocyte killing in vitro and in vivo, impedes the innate immune response to the infection, and increases fungal virulence and organ invasion in vivo. Thus, recognition of pH-regulated antigen 1 protein (Pra1p) by α(M)β₂ plays a pivotal role in determining fungal virulence and host response and protection against C. albicans infection.
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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.