ArticleThe Journal of experimental medicine2016
E3 ubiquitin ligase Cbl-b negatively regulates C-type lectin receptor-mediated antifungal innate immunity.
Article in The Journal of experimental medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed.
- Article
- The pathogenicity and future treatment strategies ofFrontiers in cellular and infection microbiology · 2026Review
- Cbl promotes MyD88 ubiquitin-mediated degradation in macrophages via phosphorylation and calcium mobilization.Frontiers in immunology · 2025Article
- The Dectin-1 and Dectin-2 clusters: C-type lectin receptors with fundamental roles in immunity.EMBO reports · 2024Review
- Intracellular checkpoints for NK cell cancer immunotherapy.Frontiers of medicine · 2024Review
- Innate immune signal transduction pathways to fungal infection: Components and regulation.Cell insight · 2024Review
- E3 ubiquitin ligase CBLB regulates innate immune responses and bacterial dissemination during nontuberculous mycobacteria infection.Journal of leukocyte biology · 2024Article
- C-type lectin receptors in antifungal immunity: Current knowledge and future developments.Parasite immunology · 2023Review
- Phagosomal signalling of the C-type lectin receptor Dectin-1 is terminated by intramembrane proteolysis.Nature communications · 2022Article
- TRIM31 facilitates K27-linked polyubiquitination of SYK to regulate antifungal immunity.Signal transduction and targeted therapy · 2021Article
- HECT E3 Ubiquitin Ligase Nedd4 Is Required for Antifungal Innate Immunity.Journal of immunology (Baltimore, Md. : 1950) · 2021Article
- MYO1F regulates antifungal immunity by regulating acetylation of microtubules.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- E3 ligase c-Cbl regulates intestinal inflammation through suppressing fungi-induced noncanonical NF-κB activation.Science advances · 2021Article
- E3 ubiquitin ligase Casitas B lineage lymphoma-b and its potential therapeutic implications for immunotherapy.Clinical and experimental immunology · 2021Review
- NR4A1 counteracts JNK activation incurred by ER stress or ROS in pancreatic β-cells for protection.Journal of cellular and molecular medicine · 2020Article
- The first line of defense: effector pathways of anti-fungal innate immunity.Current opinion in microbiology · 2020Review
- The Ubiquitin-Modifying Enzyme A20 Terminates C-Type Lectin Receptor Signals and Is a Suppressor of Host Defense against Systemic Fungal Infection.Infection and immunity · 2020Article
- Article
- Cellular and molecular mechanisms of antifungal innate immunity at epithelial barriers: The role of C-type lectin receptors.European journal of immunology · 2020Review
- Article
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Authors and funding
11 authors.
Funding
Abstract
Activation of various C-type lectin receptors (CLRs) initiates potent proinflammatory responses against various microbial infections. However, how activated CLRs are negatively regulated remains unknown. In this study, we report that activation of CLRs Dectin-2 and Dectin-3 by fungi infections triggers them for ubiquitination and degradation in a Syk-dependent manner. Furthermore, we found that E3 ubiquitin ligase Casitas B-lineage lymphoma protein b (Cbl-b) mediates the ubiquitination of these activated CLRs through associating with each other via adapter protein FcR-γ and tyrosine kinase Syk, and then the ubiquitinated CLRs are sorted into lysosomes for degradation by an endosomal sorting complex required for transport (ESCRT) system. Therefore, the deficiency of either Cbl-b or ESCRT subunits significantly decreases the degradation of activated CLRs, thereby resulting in the higher expression of proinflammatory cytokines and inflammation. Consistently, Cbl-b-deficient mice are more resistant to fungi infections compared with wild-type controls. Together, our study indicates that Cbl-b negatively regulates CLR-mediated antifungal innate immunity, which provides molecular insight for designing antifungal therapeutic agents.
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