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Open AccessJournal ArticleDOI

Signaling by Toll-like Receptors 8 and 9 Requires Bruton's Tyrosine Kinase

TLDR
Btk is established as a key signaling molecule that interacts with and acts downstream of TLR8 and TLR9, and peripheral blood mononuclear cells from patients with X-linked agammaglobulinaemia that have dysfunctional Btk are impaired in the induction of interleukin-6 by CpGB-DNA.
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This article is published in Journal of Biological Chemistry.The article was published on 2007-12-21 and is currently open access. It has received 111 citations till now. The article focuses on the topics: Bruton's tyrosine kinase & Tyrosine kinase.

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Citations
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Molecular Mechanisms That Influence the Macrophage M1–M2 Polarization Balance

TL;DR: Identification of the molecules associated with the dynamic changes of macrophage polarization and understanding their interactions is crucial for elucidating the molecular basis of disease progression and designing novel macrophages-mediated therapeutic strategies.
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Bruton's tyrosine kinase (Btk): function, regulation, and transformation with special emphasis on the PH domain.

TL;DR: Novel mutations in the pleckstrin homology domain investigated for their transforming capacity are described and it is shown that the mutant D43R behaves similar to E41K, already known to possess such activity.
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Role of Bruton's tyrosine kinase in B cells and malignancies

TL;DR: Efficacy of BTK inhibition as a single agent therapy is strong, but resistance may develop, fueling the development of combination therapies that improve clinical responses and highlighting the importance ofBTK inhibition in cancer therapy.
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Primary B Cell Immunodeficiencies: Comparisons and Contrasts

TL;DR: Identifying the genetic and environmental factors that influence the clinical phenotype may enhance patient care and the understanding of normal B cell development.
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When Signaling Pathways Collide: Positive and Negative Regulation of Toll-like Receptor Signal Transduction

TL;DR: These recent findings emphasize the importance of considering TLR signaling in the context of other signaling pathways, as is likely to occur in vivo during infection and inflammation.
References
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Journal ArticleDOI

A Toll-like receptor recognizes bacterial DNA.

TL;DR: It is shown that cellular response to CpG DNA is mediated by a Toll-like receptor, TLR9, and vertebrate immune systems appear to have evolved a specific Toll- like receptor that distinguishes bacterial DNA from self-DNA.
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Function and activation of NF-kappa B in the immune system.

TL;DR: The inhibition of NF-kappa B activation by antioxidants and specific protease inhibitors may provide a pharmacological basis for interfering with these acute processes in suppressing toxic/septic shock, graft-vs-host reactions, acute inflammatory reactions, severe phase response, and radiation damage.
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Species-Specific Recognition of Single-Stranded RNA via Toll-like Receptor 7 and 8

TL;DR: It is shown that guanosine (G)- and uridine (U)-rich ssRNA oligonucleotides derived from human immunodeficiency virus–1 (HIV-1) stimulate dendritic cells and macrophages to secrete interferon-α and proinflammatory, as well as regulatory, cytokines, and these data suggest that ssRNA represents a physiological ligand for TLR7 and TLR8.
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Innate antiviral responses by means of TLR7-mediated recognition of single-stranded RNA.

TL;DR: These results identify ssRNA as a ligand for TLR7 and suggest that cells of the innate immune system sense endosomal ssRNA to detect infection by RNA viruses.
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The family of five: TIR-domain-containing adaptors in Toll-like receptor signalling

TL;DR: The function of the fifth adaptor, SARM, has been revealed, which negatively regulates TRIF, and it is shown that it acts as a bridging adaptor in the initiation of TLR signalling.
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