ArticleProceedings of the National Academy of Sciences of the United States of America2024
BLNK negatively regulates innate antifungal immunity through inhibiting c-Cbl-mediated macrophage migration.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Maturation-Dependent Constraints in the Ability of Human Monocytes to Initiate Trained Immunity.MedComm · 2026Article
- Gut microbiota-activated PLCγ2 monocytes drive atrial fibrillation.Nature communications · 2026Article
- Non-receptor tyrosine kinase c-Abl downstream of C-type lectin receptors regulates innate antifungal immunity through c-Cbl/MAPK pathway.Infection and immunity · 2026Article
- Disseminated histoplasmosis diagnosed by mNGS in a middle-aged immunocompetent patient: a case report and literature review.BMC infectious diseases · 2026Review
- Multi-omics characterization of anoikis-related hub genes and macrophage-centered immune persistence with validation of HAVCR2 in atherosclerosis.Frontiers in immunology · 2026Article
- Expression and regulation network of BLNK in CP/CPPS in animal, cell model and clinical samples.Inflammation · 2025Article
- The role of nucleic acid sensors in antifungal immunity.Frontiers in immunology · 2025Review
- Cbl promotes MyD88 ubiquitin-mediated degradation in macrophages via phosphorylation and calcium mobilization.Frontiers in immunology · 2025Article
Corrections and comments
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Authors and funding
9 authors.
Funding
Abstract
B cell linker protein (BLNK) is crucial for orchestrating B cell receptor-associated spleen tyrosine kinase (Syk) signaling. However, the role of BLNK in Syk-coupled C-type lectin receptor (CLR) signaling in macrophages remains unclear. Here, we delineate that CLRs govern the Syk-mediated activation of BLNK, thereby impeding macrophage migration by disrupting podosome ring formation upon stimulation with fungal β-glucans or α-mannans. Mechanistically, BLNK instigates its association with casitas B-lineage lymphoma (c-Cbl), competitively impeding the interaction between c-Cbl and Src-family kinase Fyn. This interference disrupts Fyn-mediated phosphorylation of c-Cbl and subsequent c-Cbl-associated F-actin assembly. Consequently, BLNK deficiency intensifies CLR-mediated recruitment of the c-Cbl/phosphatidylinositol 3-kinase complex to the F-actin cytoskeleton, thereby enhancing macrophage migration. Notably, mice with monocyte-specific BLNK deficiency exhibit heightened resistance to infection with
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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 Socratic graph.