Evasion of Toll-like receptor 5 by flagellated bacteria.

By E. Andersen-Nissen, Kelly D. Smith, Katie L Strobe, S. L. R. Barrett, B. Cookson, S. Logan, Alan Aderem. Proceedings of the National Academy of Sciences of the United States of America, 2005

692 citations recorded by the source corpus.

Subfields: Endocrinology, Infectious Diseases, Public Health, Environmental and Occupational Health

View Paper: https://www.semanticscholar.org/paper/28d538f970cb8eee973ec27cc11e4ca9deb0265e

How researchers see this paper

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

In Endocrinology

1. Shizuo Akira
2. O. Takeuchi
3. David Mackey
4. A. Bent
5. S. Lebeer
6. J. Vanderleyden

In Infectious Diseases

1. Shizuo Akira
2. S. Lebeer
3. T. Mogensen
4. Edward A. Miao
5. J. Vanderleyden

In Public Health, Environmental and Occupational Health

1. Shizuo Akira

Citations in the corpus

• Toll-like receptors and innate immunity (2006, background): “A recent work has reported that some commensal bacteria, such as a and e Proteobacteria, change the TLR5 recognition site of flagellin without losing flagellar motility [21].”
• Comprehending crystalline β-carotene accumulation by comparing engineered cell models and the natural carotenoid-rich system of citrus (2011, neutral): “This is the result of additional mutations outside the recognized domain that preserve bacterial mobility (Andersen-Nissen et al., 2005).”
• Pathogen Recognition and Inflammatory Signaling in Innate Immune Defenses (2009, background): “In contrast, TLR5 has a stop codon variant (TLR5 392STOP) that is associated with increased susceptibility to pneumonia caused by L. pneumophila (117).”
• Host interactions of probiotic bacterial surface molecules: comparison with commensals and pathogens (2010, background): “Both the conserved flagellin MAMP and the interaction site on TLR5 have been characterize”
• Pathogen recognition and innate immunity. (2006, positive): “Certain pathogens have modified forms of the normal TLR ligands, such as the LPSs from H. pylori, P. gingivalis, and L. pneumophila and flagellin of H. pylori and C. jejuni (Andersen-Nissen et al., 2005).”
• Innate immune detection of the type III secretion apparatus through the NLRC4 inflammasome (2010, background): “Interestingly, Helicobacter pylori flagellin contains mutations that confer TLR5 evasion, however, compensatory mutations elsewhere within the flagellin protein are required to restore the ability of the protein to polymerize (29).”
• Campylobacter jejuni: molecular biology and pathogenesis (2007, background): “fcgi?db=protein&id=16751843">TLR-5 owing to key alterations in the flagellin primary structure relative to that of TLR-5-stimulatory flagellin”
• Elicitors, effectors, and R genes: the new paradigm and a lifetime supply of questions. (2007, background): “Yet a small number of pathogen species have been identified that carry sufficiently different amino acid sequences in these flagellin domains to escape detection by the host (9, 56, 137, 164).”
• Helicobacter pylori and Gastric Cancer: Factors That Modulate Disease Risk (2010, background): “pylori FlaA has low intrinsic activity to activate Toll-like receptor 5 (TLR5), which may contribute to evasion of the host immune response and to persistent colonization (15, 114, 170).”