ArticleThe Journal of allergy and clinical immunology2012
Toll-like receptor 4-, 7-, and 8-activated myeloid cells from patients with X-linked agammaglobulinemia produce enhanced inflammatory cytokines.
Article in The Journal of allergy and clinical immunology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 52 citations in OpenAlex.
- The contribution of BTK signaling in myeloid cells to neuroinflammation.Frontiers in immunology · 2025Article
- Advancements in research on the cardiovascular toxicity caused by TEC family kinases inhibitors.Frontiers in pharmacology · 2025Review
- Hematopoietic stem cell gene editing rescues B-cell development in X-linked agammaglobulinemia.The Journal of allergy and clinical immunology · 2024Article
- Dysregulation of Toll-Like Receptor Signaling-Associated Gene Expression in X-Linked Agammaglobulinemia: Implications for Correlations Genotype-Phenotype and Disease Expression.Journal of innate immunity · 2024Article
- Phenotype of BTK-lacking myeloid cells during prolonged COVID-19 and upon convalescent plasma.European journal of haematology · 2023Article
- Clinical features and mutational analysis of X-linked agammaglobulinemia patients in Malaysia.Frontiers in immunology · 2023Article
- Enhanced Bruton's tyrosine kinase activity in the kidney of patients with IgA nephropathy.International urology and nephrology · 2021Article
- Effective, safe, and sustained correction of murine XLA using a UCOE-BTK promoter-based lentiviral vector.Molecular therapy. Methods & clinical development · 2021Article
- The Clinical Course of COVID-19 Pneumonia in a 19-Year-Old Man on Intravenous Immunoglobulin Replacement Therapy for X-Linked Agammaglobulinemia.The American journal of case reports · 2021Article
- Cumulative Roles for Epstein-Barr Virus, Human Endogenous Retroviruses, and Human Herpes Virus-6 in Driving an Inflammatory Cascade Underlying MS Pathogenesis.Frontiers in immunology · 2021Article
- Multifaceted Immunomodulatory Effects of the BTK Inhibitors Ibrutinib and Acalabrutinib on Different Immune Cell Subsets - Beyond B Lymphocytes.Frontiers in cell and developmental biology · 2021Review
- Role of Host Immune and Inflammatory Responses in COVID-19 Cases with Underlying Primary Immunodeficiency: A Review.Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2020Review
- Bruton's Tyrosine Kinase Inhibition Promotes Myelin Repair.Brain plasticity (Amsterdam, Netherlands) · 2020Article
- Two X-linked agammaglobulinemia patients develop pneumonia as COVID-19 manifestation but recover.Pediatric allergy and immunology : official publication of the European Society of Pediatric Allergy and Immunology · 2020Article
- Distinct Clinical Features and Novel Mutations in Taiwanese Patients With X-Linked Agammaglobulinemia.Frontiers in immunology · 2020Article
- Fatal Progressive Meningoencephalitis Diagnosed in Two Members of a Family With X-Linked Agammaglobulinemia.Frontiers in pediatrics · 2020Article
- Role of Bruton's tyrosine kinase in B cells and malignancies.Molecular cancer · 2018Review
- Type I and III Interferon Productions Are Impaired in X-Linked Agammaglobulinemia Patients Toward Poliovirus but Not Influenza Virus.Frontiers in immunology · 2018Article
- Periodontal and other oral manifestations of immunodeficiency diseases.Oral diseases · 2017Review
- Bruton's Tyrosine Kinase, a Component of B Cell Signaling Pathways, Has Multiple Roles in the Pathogenesis of Lupus.Frontiers in immunology · 2017Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 2 countries.
Funding
Abstract
backgroundBruton tyrosine kinase (BTK) is a component of signaling pathways downstream from Toll-like receptors (TLRs) 2, 4, 7, 8, and 9. Previous work in BTK-deficient mice, cell lines, and cultured cells from patients with X-linked agammaglobulinemia (XLA) suggested defective TLR-driven cytokine production.
objectiveWe sought to compare TLR-4-, TLR-7-, and TLR-8-induced cytokine production of primary cells from patients with XLA with that seen in control cells.
methodsPBMCs from patients with XLA, freshly isolated plasmacytoid dendritic cells, monocytes, and monocytoid dendritic cells were activated with TLR-4, TLR-7, and TLR-8 agonists. Signaling intermediates and intracellular and secreted cytokine levels were compared with those seen in control cells.
resultsAlthough TLR-4, TLR-7, and TLR-8 activation of nuclear factor κB and mitogen-activated protein kinase pathways in cells from patients with XLA and control cells were comparable, TLR-activated freshly isolated monocytes and monocytoid dendritic cells from patients with XLA produced significantly more TNF-α, IL-6, and IL-10 than control cells. TLR-7/8-activated plasmacytoid dendritic cells produced normal amounts of IFN-α. In murine models BTK regulates the degradation of Toll-IL-1 receptor domain-containing adaptor protein, terminating TLR-4-induced cytokine production. Although this might explain the heightened TLR-4-driven cytokine production we observed, Toll-IL-1 receptor domain-containing adaptor protein degradation is intact in cells from patients with XLA, excluding this explanation.
conclusionIn contrast to previous studies with BTK-deficient mice, cell lines, and cultured cells from patients with XLA suggesting impaired TLR-driven cytokine production, these data suggest that BTK inhibits TLR-induced cytokine production in primary human cells.
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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.