Essential role of MD-2 in LPS responsiveness and TLR4 distribution

By Y. Nagai, S. Akashi, M. Nagafuku, M. Ogata, Y. Iwakura, Shizuo Akira, T. Kitamura, A. Kosugi, M. Kimoto, K. Miyake. Nature Immunology, 2002

1,120 citations recorded by the source corpus.

Subfields: Immunology, Pulmonary and Respiratory Medicine

View Paper: https://www.semanticscholar.org/paper/f8e1fd625f5f3c75b1c3c8dc01b721cacd8d193b

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In Immunology

1. Shizuo Akira
2. B. Beutler
3. K. Takeda
4. Taro Kawai
5. T. Kaisho
6. Kui Li
7. Sandra N. Lester
8. K. Hoebe

Citations in the corpus

• European Position Paper on Rhinosinusitis and Nasal Polyps 2012. (2012, background): “In another uncontrolled trial 40 patients altogether were treated with either roxithromycin 150 mg alone or in combination with an antihistamine (azelastine) for at least 8 weeks. Smaller polyps were more likely to shrink and this happened in about half of the patients ((1702)).”
• Co-operation of TLR4 and raft proteins in LPS-induced pro-inflammatory signaling (2014, background): “By simultaneously binding to MD-2 and to the adjacent TLR4 receptor, LPS facilitates formation of ‘‘M’’ shaped dimers of TLR4/MD-2 complexes [8, 20–22].”
• Innate Immune Pattern Recognition: A Cell Biological Perspective (2015, neutral): “MD-2 is required for TLR4 dimerization in response to LPS and is therefore essential for all TLR4-dependent responses to bacteria (60, 61).”
• IL-6 induces an anti-inflammatory response in the absence of SOCS3 in macrophages (2003, methodology): “Mice were challenged intraperitoneally with 250 ng of LPS ( Escherichia coli serotype 055:B5, Sigma) and 25 mg of galactosamine (Sigma”
• Toll-like receptors. (2003, background): “Whereas TLR4 normally resides on the cell surface in wild-type cells, it is found in the Golgi apparatus in cells deficient for MD-2, indicating that MD-2 is essential for the intracellular distribution of TLR4 (47).”
• Crystal structure of the TLR4-MD-2 complex with bound endotoxin antagonist Eritoran. (2007, positive): “However, transfection of TLR4 alone is not enough for LPS recognition, and physical association of TLR4 with MD-2 on the cell surface is a prerequisite for ligand-induced activation (Nagai et al., 2002; Schromm et al., 2001; Shimazu et al., 1999).”
• Innate immune sensing and its roots: the story of endotoxin (2003, background): “96 ), and Miyake and colleagues, as well as others, later proved definitively that this interaction is essential for LPS signallin”
• Receptors, Mediators, and Mechanisms Involved in Bacterial Sepsis and Septic Shock (2003, background): “MD-2 as essential accessory molecules in TLR4-mediated signaling and intracellular trafficking (379, 487), whereas MD-1 is”
• How we detect microbes and respond to them: the Toll‐like receptors and their transducers (2003, background): “Finally, a small, exteriorized molecule known as MD-2 was shown to be an essential part of the receptor complex [10, 11].”
• Toll-like receptors in antiviral innate immunity (2013, background): “MD-2 deficiency in mice augments susceptibility to infection and diminishes their response to LPS [176].”
• LPS, TLR4 and infectious disease diversity (2005, background): “The importance of TLR4, CD14 and MD2 in LPS recognition is highlighted by the unresponsive phenotype of mice carrying knockout mutations in any of these genes and the fact that, in humans, polymorphisms in these genes reduce the magnitude of LPS response”