Pathogen recognition with Toll-like receptors.
By Taro Kawai, Shizuo Akira. Current Opinion in Immunology, 2005
632 citations recorded by the source corpus.
Subfields: Epidemiology, Immunology
View Paper: https://www.semanticscholar.org/paper/693a2030fb600871ce3d6537b38145cb4333f65a
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In Epidemiology
In Immunology
Citations in the corpus
- Periodontitis: a polymicrobial disruption of host homeostasis (2010, background): “recognize microbial components (such as DNA, flagella and fimbriae) that are shared by oral commensal and periopathogenic species and recognize peptidoglycan and lipoteichoic acids in Gram-positive bacteria as well as lipopolysaccharide in Gram-negative bacteria, and they then activate various innat”
- Obesity, Inflammation, Toll-Like Receptor 4 and Fatty Acids (2018, background): “This phosphorylation results in IκB dissociation from the NF-κB complex and its subsequent polyubiquitination, which, in turn, leads to IkB degradation (mediated by the 26S proteasome) [73,81].”
- Systems biology approaches identify ATF3 as a negative regulator of Toll-like receptor 4 (2006, background): “In equation (1), the term Il6 represents the level of Il6 mRNA expression as”
- Anti-immunology: evasion of the host immune system by bacterial and viral pathogens. (2006, background): “At present, 10 TLRs are expressed in man and 12 in the mouse, and many have been assigned viral PAMPs that can be recognized as ligands (Bowie and Haga, 2005; Kawai and Akira, 2005).”