ArticleThe Journal of infectious diseases2018
A Dectin-1-Caspase-8 Pathway Licenses Canonical Caspase-1 Inflammasome Activation and Interleukin-1β Release in Response to a Pathogenic Fungus.
Article in The Journal of infectious diseases, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
What it found
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Who cites it
15 citing papers in PubMed, 26 citations in OpenAlex.
- Cytosolic receptors and signaling in antifungal immunity.The EMBO journal · 2025Review
- Evidence for a RIPK1-independent survival mechanism for CASPASE-8 in αβ T cells.Discovery immunology · 2025Article
- Crosstalk of pyroptosis and cytokine in the tumor microenvironment: from mechanisms to clinical implication.Molecular cancer · 2024Review
- INPP5D regulates inflammasome activation in human microglia.Nature communications · 2023Article
- Genome-Wide Association Study RevealsJournal of fungi (Basel, Switzerland) · 2023Article
- Involvement of inflammasomes in tumor microenvironment and tumor therapies.Journal of hematology & oncology · 2023Review
- Article
- Role for IL-1 Family Cytokines in Fungal Infections.Frontiers in microbiology · 2021Review
- The first line of defense: effector pathways of anti-fungal innate immunity.Current opinion in microbiology · 2020Review
- Caspase-8 mediates inflammation and disease in rodent malaria.Nature communications · 2020Article
- Inflammasome signaling and regulation of interleukin-1 family cytokines.The Journal of experimental medicine · 2020Review
- Caspase-11-dependent IL-1α release boosts Th17 immunity against Paracoccidioides brasiliensis.PLoS pathogens · 2019Article
- Involvement of the Dectin-1 Receptor upon the Effector Mechanisms of Human Phagocytic Cells againstJournal of immunology research · 2019Article
- Review
- Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
Background: Paracoccidioides brasiliensis is equipped with an arsenal of virulence factors that are crucial for causing infection. Our group previously defined the NLRP3 inflammasome as a mediator of P brasiliensis-induced cell damage recognition and induction of effective Th1 immune responses. However, deficiency of caspase-1 only partially reduced interleukin (IL)-1β levels. Methods: In this study, using chemical inhibitors as well as genetically modified mice, we identify an additional pathway for IL-1β production in response to P brasiliensis infection. Results: Paracoccidioides brasiliensis initiated caspase-8-mediated IL-1β production, an event that was necessary for transcriptional priming and posttranslational processing of pro-IL-1β. Caspase-8 synergizes with the canonical NLRP3 inflammasome pathway to control caspase-1 processing and IL-1β maturation, providing a regulatory role for caspase-8 in host resistance to in vivo P brasiliensis infection. Conclusions: Taken together, these findings revealed an important role for caspase-8 in the innate immune response of host cells to P brasiliensis infection, demonstrating a connected network between noncanonical and canonical inflammasomes to coordinate IL-1β production during fungal challenge.
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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.