Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Cutting edge: TLR2-deficient and MyD88-deficient mice are highly susceptible to Staphylococcus aureus infection.

Journal of immunology (Baltimore, Md. : 1950) - 15 Nov 2000

Takeuchi O, Hoshino K, Akira S

Abstract excerpt

Toll-like receptor (TLR) family acts as pattern recognition receptors for pathogen-specific molecular patterns. We previously showed that TLR2 recognizes Gram-positive bacterial components whereas TLR4 recognizes LPS, a component of Gram-negative bacteria. MyD88 is shown to be an adaptor molecule essential for TLR family signaling. To investigate the role of TLR family in host defense against Gram-positive...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Antigens, Differentiation
Share to Macrophages, Peritoneal

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Myeloid Differentiation Factor 88

Share to Receptors, Immunologic

Share to Staphylococcal Infections

Share to Toll-Like Receptor 2

Share to Toll-Like Receptor 4

Share to Toll-Like Receptors

Source

Identifiers

PMID: 11067888
DOI: 10.4049/jimmunol.165.10.5392

Genes

TLR2
TLR4

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Cutting edge: TLR2-deficient and MyD88-deficient mice are highly susceptible to Staphylococcus aureus infection.PMID 11067888Read ↗

Toll-like receptors are temporally involved in host defense.Semantic proximity Read ↗

Cutting edge: myeloid differentiation factor 88 is essential for pulmonary host defense against Pseudomonas aeruginosa but not Staphylococcus aureus.Semantic proximity Read ↗

How important are Toll-like receptors for antimicrobial responses?Semantic proximity Read ↗

Role of the innate immune system in host defence against bacterial infections: focus on the Toll‐like receptorsSemantic proximity Read ↗

A Staphylococcus aureus TIR domain protein virulence factor blocks TLR2-mediated NF-κB signaling.Semantic proximity Read ↗

MyD88-dependent but Toll-like receptor 2-independent innate immunity to Listeria: no role for either in macrophage listericidal activity.Semantic proximity Read ↗

The importance of Toll-like receptor 2 polymorphisms in severe infections.Semantic proximity Read ↗

The function of TLR2 during staphylococcal diseasesSemantic proximity Read ↗

The development of early host response to Pseudomonas aeruginosa lung infection is critically dependent on myeloid differentiation factor 88 in mice.Semantic proximity Read ↗

TLR2 signalling: At the crossroads of commensalism, invasive infections and toxic shock syndrome by Staphylococcus aureusSemantic proximity Read ↗

Mal, more than a bridge to MyD88Semantic proximity Read ↗

Dual role of TLR2 and myeloid differentiation factor 88 in a mouse model of invasive group B streptococcal disease.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.