Human Toll-like receptor 4 recognizes host-specific LPS modifications

By A. Hajjar, R. Ernst, J. Tsai, Christopher B Wilson, Samuel I. Miller. Nature Immunology, 2002

625 citations recorded by the source corpus.

Subfields: Epidemiology, Immunology, Pulmonary and Respiratory Medicine

View Paper: https://www.semanticscholar.org/paper/cf77874169c2852effbf1704065709cde8ab79f0

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In Epidemiology

1. Shizuo Akira
2. K. Takeda
3. Curtis Huttenhower
4. Y. Iwakura
5. Ramnik J. Xavier
6. B. Cookson
7. R. Medzhitov
8. Taro Kawai

In Immunology

1. Shizuo Akira
2. K. Takeda
3. T. Kaisho
4. R. Medzhitov
5. K. Kwiatkowska
6. Taro Kawai
7. Yuanqing Liu
8. Céline Vaure

Citations in the corpus

• Variation in Microbiome LPS Immunogenicity Contributes to Autoimmunity in Humans. (2016, positive): “One limitation of mouse studies is that LPS subtypes that are antagonistic or silent in humans are instead recognized as stimulatory in mice due to differences between the mouse and human LPS co-receptor MD2 (Hajjar et al., 2002).”
• A Comparative Review of Toll-Like Receptor 4 Expression and Functionality in Different Animal Species (2014, background): “This discrimination is mediated by the 82-amino acid hypervariable region of TLR4 (44).”
• TLR4 and CD14 trafficking and its influence on LPS-induced pro-inflammatory signaling (2020, background): “Deacylation and dephosphorylation of LPS deprived it of a pro-inflammatory activity especially in human cells [59, 61], due to a weaker or no activation of human TLR4 by these LPS species, as discussed above.”
• Toll-like receptors. (2003, background): “This is in sharp contrast to TLR1, TLR2, and TLR4, which are expressed on the cell surface (44, 75, 135, 136).”
• Essential role of MD-2 in LPS responsiveness and TLR4 distribution (2002, background): “, and both TLR4 and MD-2 likely recognize ligands, as has been reporte”
• Crystal structure of the TLR4-MD-2 complex with bound endotoxin antagonist Eritoran. (2007, positive): “It includes the ‘‘hypervariable’’ region that is essential for recognition of an LPS variant from P. aeruginosa ( Hajjar et al., 2002 ).”
• Toll-like receptor 5 recognizes a conserved site on flagellin required for protofilament formation and bacterial motility (2003, background): “In addition, our data indicate that TLR5 most likely directly interacts with flagellin, and that species-specific differences in TLR5 sequence dictate fine specificity for flagellin molecules, as is hypothesized for TLR4 recognition of LP”
• LPS, TLR4 and infectious disease diversity (2005, methodology): “aeruginosa lipid A structures by mice and humans by the use of receptor chimaera”
• Pathophysiology and management of pulmonary infections in cystic fibrosis. (2003, background): “aeruginosa adaptation within the CF airway is associated with modifications to LPS structure (95, 96); the specific LPS structures required for P.”
• Pseudomonas aeruginosa: pathogenesis, virulence factors, antibiotic resistance, interaction with host, technology advances and emerging therapeutics (2022, background): “Research shows that a large amount of hex-acylated lipid A from LPS is isolated from infected patients, which is a strong TLR4 agonist, capable of activating TLR4-dependent inflammatory response.(271,272) In addition, several TLR4 co-receptors MD-2 and CD14 are indicated necessary for TLR4 recogniti”