CD14 is required for MyD88-independent LPS signaling

By Zhengfan Jiang, P. Georgel, Xin Du, L. Shamel, Sosathya Sovath, Suzanne Mudd, M. Huber, C. Kalis, S. Keck, C. Galanos and 2 more. Nature Immunology, 2005

742 citations recorded by the source corpus.

Subfields: Immunology

View Paper: https://www.semanticscholar.org/paper/de703cd7b3e2b8b4941f0df4483bacfae50b0c06

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In Immunology

1. Shizuo Akira
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Citations in the corpus

• Innate Immune Pattern Recognition: A Cell Biological Perspective (2015, neutral): “This process of receptor endocytosis is critical for regulating TLR4-mediated type I IFN production (discussed in more detail in the following section), which specifically occurs from endosomes (23, 71), and it also explains previous reports that CD14 is required for LPS-mediated IFN production (72)”
• Microbial stimulation fully differentiates monocytes to DC-SIGN/CD209+ dendritic cells for immune T cell areas (2010, background): “We then compared mice lacking the MyD88 and Trif adaptors for TLR4 signaling, where CD14 is a known coreceptor for MyD88-independent, Trif-dependent signaling (Jiang et al., 2005).”
• Crystal structure of the TLR4-MD-2 complex with bound endotoxin antagonist Eritoran. (2007, positive): “CD14 is indispensable for physiological response of LPS by catalyzing binding of LPS to the TLR4-MD-2 complex and by modulating signaling activity of LPS (Haziot et al., 1995; Jiang et al., 2005; Miyake, 2006).”
• Apoptotic caspases prevent the induction of type I interferons by mitochondrial DNA (2014, methodology): “Type I IFN Bioassay To measure type I IFN bioactivity, undiluted culture supernatants were transferred on cultures of the L929-pISRE-Luc reporter cell line (Jiang et al., 2005).”
• CD14 controls the LPS-induced endocytosis of Toll-like Receptor 4 (2011, background): “In contrast, if CD14 must physically change the conformation of TLR4 to permit TRIF signaling (Jiang et al., 2005), then altering TLR4 localization would not restore IFN expression to CD14-deficient cells.”
• ERIS, an endoplasmic reticulum IFN stimulator, activates innate immune signaling through dimerization (2009, methodology): “Type I IFN activity was measured as previously described (34), with reference to a recombinant human IFN- (R & D Systems) standard using a 2FTGH cell line (1 105 cells/mL) stably transfected with an IFNsensitive (ISRE) luciferase construct.”
• Peroxisomes are signaling platforms for antiviral innate immunity (2010, neutral): “Type I IFN activity was measured as described (Jiang et al., 2005).”
• Co-operation of TLR4 and raft proteins in LPS-induced pro-inflammatory signaling (2014, methodology): “the involvement of CD14 was found to differently determine TLR4 responses to so-called smooth (s) and rough (r) chemotypes of LPS [88].”
• TLR4 and CD14 trafficking and its influence on LPS-induced pro-inflammatory signaling (2020, background): “Accordingly, the TRIF-dependent signaling was abolished, while the MyD88-dependent one was not affected by the CD14 depletion especially in cells stimulated with so-called rough chemotype (devoid of the O-polysaccharide chain) of LPS [31, 32, 34].”
• Tenascin-C is an endogenous activator of Toll-like receptor 4 that is essential for maintaining inflammation in arthritic joint disease (2009, neutral): “As a positive control, here we examined the activity of smooth glycosylated LPS, which requires both MD-2 and CD14 for its actio”