Toll-like receptor 4 imparts ligand-specific recognition of bacterial lipopolysaccharide.

By E. Lien, T. Means, H. Heine, A. Yoshimura, S. Kusumoto, K. Fukase, M. Fenton, M. Oikawa, N. Qureshi, Brian G. Monks and 3 more. Journal of Clinical Investigation, 2000

795 citations recorded by the source corpus.

Subfields: Immunology, Nutrition and Dietetics, Pulmonary and Respiratory Medicine

View Paper: https://www.semanticscholar.org/paper/56d3e692c09391ceb89556d91ff0869c0dd80f26

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Immunology

1. Shizuo Akira
2. R. Medzhitov
3. K. Takeda
4. Taro Kawai
5. B. Beutler
6. S. Ghosh
7. T. Kaisho
8. D. Underhill

In Nutrition and Dietetics

1. R. Medzhitov

Citations in the corpus

• Toll-like receptor 5 recognizes a conserved site on flagellin required for protofilament formation and bacterial motility (2003, background): “Direct interaction between TLR4 and lipopolysaccharide (LPS) has been postulated based on genetic studie”
• Toll-like receptors and innate immunity (2001, background): “Several lines of evidence indicate that TLR4 might, in fact, interact with LPS directl”
• Regulation of Tau Pathology by the Microglial Fractalkine Receptor (2010, positive): “LPS is an endotoxin that is part of the outer wall of Gram-negative bacteria and can induce systemic inflammation via engagement of TLR4 (Lien et al., 2000).”
• Toll-like receptors in the induction of the innate immune response (2000, background): “Recent results suggest that the fatty-acid composition might dictate the binding specificities of key receptor”
• The evolution and genetics of innate immunity (2001, background): “In further genetic studies of LPS responses, it was demonstrated that the species origin of Tlr4 was entirely responsible for species-specific responses to certain LPS partial structure”
• Toll-like receptors: critical proteins linking innate and acquired immunity (2001, background): “When the TLR4 from one species is expressed in cells from a different species, the response to lipid A is determined by the introduced TLR, not that of the host cell”
• Signaling by Toll-Like Receptor 2 and 4 Agonists Results in Differential Gene Expression in Murine Macrophages (2001, background): “In contrast, CHO cells engineered to express the reporter construct, CD14, and human TLR2 (14, 15 ) responded to all three stimuli to express Tac antigen (H. Heine, personal communication).”
• Essential role of MD-2 in LPS responsiveness and TLR4 distribution (2002, background): “TLR4 also contributes to species-specific recognition of lipid IV”
• Toll-like receptor-mediated NF-kappaB activation: a phylogenetically conserved paradigm in innate immunity. (2001, background): “The ability of TLR4 to recognize and discriminate between the fine structural differences within the lipid A portion of LPS supports the notion that TLR4 physically interacts with lipid A (28, 29).”
• CD14 is required for MyD88-independent LPS signaling (2005, result): “Rough LPS or lipid A stimulates MyD88-dependent activation in the absence of CD14, which is consistent with the hypothesis that lipid A molecules undergo direct contact with TLR4 in order to signa”