Toll-like Receptors and Type I Interferons*
By Satoshi Uematsu, Shizuo Akira. 2007
510 citations recorded by the source corpus.
Toll-like receptors (TLRs) are key molecules of the innate immune systems, which detect conserved structures found in a broad range of pathogens and trigger innate immune responses. A subset of TLRs recognizes viral components and induces antiviral responses. Whereas TLR4 recognizes viral components at the cell surface, TLR3, TLR7, TLR8, and TLR9 recognize viral nucleic acids on endosomal membrane. After ligand recognition, these members activate their intrinsic signaling pathways and induce type I interferon. In this review, we discuss the recent findings of the viral recognition by TLRs and their signaling pathways.
Subfields: Epidemiology, Immunology
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Epidemiology
In Immunology
Citations in the corpus
- Function of Nod‐like receptors in microbial recognition and host defense (2009, background): “Toll receptors were first defined in the fruit fly and localize either at the cell surface or within endosomes (6, 7).”
- Plasmacytoid dendritic cells: sensing nucleic acids in viral infection and autoimmune diseases (2008, background): “32 ), are located in intracellular endosomal-lysosomal compartment”
- Highly efficient reprogramming to pluripotency and directed differentiation of human cells using synthetic modified mRNA (2010, background): “Cel It is known that exogenous single-stranded RNA (ssRNA) activates antiviral defenses in mammalian cells through interferonand NF-kB-dependent pathways (Diebold et al., 2004; Hornung et al., 2006; Kawai and Akira, 2007; Pichlmair et al., 2006; Uematsu and Akira, 2007).”
- Activation of innate immune antiviral response by NOD2 (2009, background): “Virus-infected cells use pattern-recognition receptors (PRRs) to recognize pathogen-associated molecular patterns (PAMPs; in this case, virus-associated molecular patterns) and to trigger phosphorylation of the transcription factor interferon-regulatory factor 3 (IRF3), which then translocates to th”