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Article

A common dominant TLR5 stop codon polymorphism abolishes flagellin signaling and is associated with susceptibility to legionnaires' disease.

The Journal of experimental medicine - 17 Nov 2003

Hawn Thomas R, Verbon Annelies, Lettinga Kamilla D, Zhao Lue Ping, Li Shuying Sue, Laws Richard J, Skerrett Shawn J, Beutler Bruce, Schroeder Lea, Nachman Alex, Ozinsky Adrian, Smith Kelly D, Aderem Alan

Abstract excerpt

Although Toll-like receptors (TLRs) are critical mediators of the immune response to pathogens, the influence of polymorphisms in this gene family on human susceptibility to infection is poorly understood. We demonstrated recently that TLR5 recognizes flagellin, a potent inflammatory stimulus pre...

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Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

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Source

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Identifiers

PMID: 14623910
DOI: 10.1084/jem.20031220
PMCID: PMC2194120

Genes

TLR5

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 1 Sept 2026. Prepared record publication-14623910-2026-09-01.1. Manifest publication-graph-cohort-2026-09-01.1.

Source receipt: PubMed via Helena Literature Corpus, retrieved 1 Sept 2026.

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A common dominant TLR5 stop codon polymorphism abolishes flagellin signaling and is associated with susceptibility to legionnaires' disease.PMID 14623910Read ↗

Characterization and functional investigation of single nucleotide polymorphisms (SNPs) in the human TLR5 gene.Semantic proximity Read ↗

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A conserved surface on Toll-like receptor 5 recognizes bacterial flagellin.Semantic proximity Read ↗

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A non-synonymous coding variant (L616F) in the TLR5 gene is potentially associated with Crohn's disease and influences responses to bacterial flagellin.Semantic proximity Read ↗

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Convergent losses of <i>TLR5</i> suggest altered extracellular flagellin detection in four mammalian lineagesSemantic proximity Read ↗

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