ReviewCurrent opinion in microbiology2016
Alarmin(g) the innate immune system to invasive fungal infections.
Review in Current opinion in microbiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
14 citing papers in PubMed.
- Article
- Microbial adaptive pathogenicity strategies to the host inflammatory environment.FEMS microbiology reviews · 2025Review
- Time-Course Transcriptomic Analysis Reveals the Crucial Roles of PANoptosis in Fungal Keratitis.Investigative ophthalmology & visual science · 2023Article
- The TLR-NF-kB axis contributes to the monocytic inflammatory response against a virulent strain ofFrontiers in immunology · 2022Article
- New, Biocompatible, Chitosan-Gelled Microemulsions Based on Essential Oils and Sucrose Esters as Nanocarriers for Topical Delivery of Fluconazole.Pharmaceutics · 2021Article
- ZBP1 promotes fungi-induced inflammasome activation and pyroptosis, apoptosis, and necroptosis (PANoptosis).The Journal of biological chemistry · 2020Article
- 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
- Mechanism of Candida pathogenesis: revisiting the vital drivers.European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 2020Review
- Host Immune Defense upon Fungal Infections with Mucorales: Pathogen-Immune Cell Interactions as Drivers of Inflammatory Responses.Journal of fungi (Basel, Switzerland) · 2020Review
- Danger signals in oral cavity-related diseases.Journal of leukocyte biology · 2019Review
- Modulation of the Fungal-Host Interaction by the Intra-Species Diversity of C. albicans.Pathogens (Basel, Switzerland) · 2018Review
- Interleukin 1α Is Critical for Resistance against Highly Virulent Aspergillus fumigatus Isolates.Infection and immunity · 2017Article
- Antifungal Therapy for Systemic Mycosis and the Nanobiotechnology Era: Improving Efficacy, Biodistribution and Toxicity.Frontiers in microbiology · 2017Review
- Prescribing Pattern of Antifungal Medications at a Tertiary Care Hospital in Oman.Journal of clinical and diagnostic research : JCDR · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
Abstract
Fungi encounter numerous stresses in a mammalian host, including the immune system, which they must adapt to in order to grow and cause disease. The host immune system tunes its response to the threat level posed by the invading pathogen. We discuss recent findings on how interleukin (IL)-1 signaling is central to tuning the immune response to the virulence potential of invasive fungi, as well as other pathogens. Moreover, we discuss fungal factors that may drive tissue invasion and destruction that regulate IL-1 cytokine release. Moving forward understanding the mechanisms of fungal adaption to the host, together with understanding how the host innate immune system recognizes invading fungal pathogens will increase our therapeutic options for treatment of invasive fungal infections.
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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.