Identification of Lps2 as a key transducer of MyD88-independent TIR signalling

By K. Hoebe, Xin Du, P. Georgel, E. Janssen, K. Tabeta, S. Kim, Jason Goode, Pei Lin, N. Mann, Suzanne Mudd and 4 more. Nature, 2003

1,370 citations recorded by the source corpus.

Subfields: Cancer Research, Immunology

View Paper: https://www.semanticscholar.org/paper/e5f1b5a5c61f0fb49b5496b24541969e0d9ac242

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Citations in the corpus

Innate immunity: an overview. (2004, background): “Not only bacteria and fungi, but protozoa (Campos et al., 2001) and viruses ( Hoebe et al., 2003a; Alexopoulou et al., 2001) are recognized by the TLRs.”
MyD88-mediated stabilization of interferon-γ-induced cytokine and chemokine mRNA (2006, neutral): “7 macrophages expressing luciferase-ARE TNF with plasmids encoding apoptosis signal–regulating kinase-1 (ASK1), MLK3, MKK3, MKK6, IRAK1, or the TIR domain–containing adapter inducing IFN-β (TRIF”
TLR4 enhances TGF-β signaling and hepatic fibrosis (2007, neutral): “Specific pathogen-free 8-week-old male TLR4–wild-type (C3H/HeOuJ), TLR4-mutant (C3H/HeJ), Tlr2 -deficient, Trif Lps2/Lps2 (ref”
Toll-like receptors activate programmed necrosis in macrophages through a receptor-interacting kinase-3–mediated pathway (2011, background): “Both TRIF-deficient and TRIF dominant-negative mutant mice are defective in activating IFN regulatory factor 3 (IRF3) nor able to induce type I IFNs in response to LPS or poly(I:C) (14, 15).”
RIP3 mediates the embryonic lethality of caspase-8-deficient mice (2011, neutral): “This resistance was comparable to the negative control TRIF-deficient mice 19 (Supplementary Fig.”
TLR3: interferon induction by double-stranded RNA including poly(I:C). (2008, background): “Contribution of TLR3 and TLR9 in antiviral responses has been shown in MCMV infection [76,82], which partly relies on NK cell activation for virus clearance.”
Toll-like receptors and innate immunity (2006, background): “A third adapter, TRIF [53, 54], is essential for the TLR3- and TLR4-mediated MyD88-independent pathway [39, 55].”
Antimicrobial activity of mucosal-associated invariant T cells (2010, methodology): “We then used BMDCs singly or doubly deficient in the adaptors MyD88 and TRIF, which are impaired in their response to many TLR ligands and IL-1&beta”