ArticlePloS one2014
Btk regulates macrophage polarization in response to lipopolysaccharide.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 83 papers.
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Who cites it
83 citing papers in PubMed, 134 citations in OpenAlex.
- Harnessing myeloid cell plasticity for cancer therapy.Nature cancer · 2026Review
- Rus-GXF, a ruscogenin glycoside, binds to the ADP-binding domain of JAK1 to prevent inflammation and barrier damage in acute lung injury.Frontiers in pharmacology · 2026Article
- Identification of Potential Nontoxic HumanACS omega · 2025Article
- Current and future landscape of Bruton tyrosine kinase inhibitors in allergy.The Journal of allergy and clinical immunology · 2025Review
- Beyond relapses: How BTK inhibitors are shaping the future of progressive MS treatment.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025Review
- Article
- Evobrutinib mitigates neuroinflammation after ischemic stroke by targeting M1 microglial polarization via the TLR4/Myd88/NF-κB pathway.Molecular medicine (Cambridge, Mass.) · 2025Article
- Identification of BTK as an immune-related biomarker for Hashimoto's thyroiditis by integrated bioinformatic analysis.BMC immunology · 2025Article
- Inhibition of BTK and SYK attenuatesJournal of oral microbiology · 2025Article
- Anti-atherosclerotic effects and molecular targets of salvianolic acids fromFrontiers in pharmacology · 2025Review
- Review
- Bruton Tyrosine Kinase Inhibition Decreases Inflammation and Differentially Impacts Phagocytosis and Cellular Metabolism in Mouse- and Human-derived Myeloid Cells.ImmunoHorizons · 2024Article
- A review of Bruton's tyrosine kinase inhibitors in multiple sclerosis.Therapeutic advances in neurological disorders · 2024Review
- Bruton's tyrosine kinase inhibition limits endotoxic shock by suppressing IL-6 production by marginal zone B cells in mice.Frontiers in immunology · 2024Article
- Differential Gene Expression of SARS-CoV-2 Positive Bronchoalveolar Lavages: A Case Series.Pathobiology : journal of immunopathology, molecular and cellular biology · 2024Article
- Disease Modifying Strategies in Multiple Sclerosis: New Rays of Hope to Combat Disability?Current neuropharmacology · 2024Review
- A Review on Role of Inflammation in Coronavirus Disease.Endocrine, metabolic & immune disorders drug targets · 2024Review
- CXCR4-BTK axis mediate pyroptosis and lipid peroxidation in early brain injury after subarachnoid hemorrhage via NLRP3 inflammasome and NF-κB pathway.Redox biology · 2023Article
- Identification of a pharyngeal mucosal lymphoid organ in zebrafish and other teleosts: Tonsils in fish?Science advances · 2023Article
- Review
23 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
11 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Bacterial Lipopolysaccharide (LPS) is a strong inducer of inflammation and does so by inducing polarization of macrophages to the classic inflammatory M1 population. Given the role of Btk as a critical signal transducer downstream of TLR4, we investigated its role in M1/M2 induction. In Btk deficient (Btk (-\-)) mice we observed markedly reduced recruitment of M1 macrophages following intraperitoneal administration of LPS. Ex vivo analysis demonstrated an impaired ability of Btk(-/-) macrophages to polarize into M1 macrophages, instead showing enhanced induction of immunosuppressive M2-associated markers in response to M1 polarizing stimuli, a finding accompanied by reduced phosphorylation of STAT1 and enhanced STAT6 phosphorylation. In addition to STAT activation, M1 and M2 polarizing signals modulate the expression of inflammatory genes via differential activation of transcription factors and regulatory proteins, including NF-κB and SHIP1. In keeping with a critical role for Btk in macrophage polarization, we observed reduced levels of NF-κB p65 and Akt phosphorylation, as well as reduced induction of the M1 associated marker iNOS in Btk(-/-) macrophages in response to M1 polarizing stimuli. Additionally enhanced expression of SHIP1, a key negative regulator of macrophage polarisation, was observed in Btk(-/-) macrophages in response to M2 polarizing stimuli. Employing classic models of allergic M2 inflammation, treatment of Btk (-/-) mice with either Schistosoma mansoni eggs or chitin resulted in increased recruitment of M2 macrophages and induction of M2-associated genes. This demonstrates an enhanced M2 skew in the absence of Btk, thus promoting the development of allergic inflammation.
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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.