Toll-like receptors and their crosstalk with other innate receptors in infection and immunity.

By Taro Kawai, Shizuo Akira. Immunity, 2011

3,620 citations recorded by the source corpus.

Subfields: Immunology, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/ac3d564501629135211f048085e3dec14827d2c1

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Citations in the corpus

Latent enhancers activated by stimulation in differentiated cells. (2013, neutral): “Stimuli included (1) two Toll-like receptor (TLR) agonists specific for TLR2 (macrophage-activating lipopeptide-2 [MALP-2]) and TLR9 (unmethylated CpGcontaining oligonucleotide) (Kawai and Akira, 2011); these stimuli differ from LPS (acting on TLR4) mainly because of their inability to induce IRF3-d”
Toll-Like Receptor Signaling Pathways (2014, background): “These findings suggest that host makes a distinction between different types of LPS-containing bacteria by activating distinct signaling pathways (79).”
IL-1 receptor antagonist ameliorates inflammasome-dependent alcoholic steatohepatitis in mice. (2012, background): “Given the partial overlap of signaling pathways downstream of TLR4 and IL-1R1 (22), we hypothesized that IL-1β augments TLR4-dependent signaling in immune cells.”
Toll-like receptors in antiviral innate immunity (2013, background): “In pDCs, they are biased toward rapid, copious production of type I IFNs [2,44].”
The crucial roles of inflammatory mediators in inflammation: A review (2018, background): “The main anti-inflammatory drugs are either steroidal [100] (e.”
Sepsis: current dogma and new perspectives. (2014, background): “…deficiency of TLR4, MD2, or HMGB1, and other molecules implicated in the sensing and signal transduction mechanisms of LPS responsiveness each confer protection against LPS-mediated TNF release, and therefore, protect against shock (O’Neill et al., 2013; Kawai and Akira, 2011; Yanai et al., 2009).”
From Monocytes to M1/M2 Macrophages: Phenotypical vs. Functional Differentiation (2014, background): “Thus, considering that macrophages recognize pathogens directly (174, 175), while T-cell do not, and considering that T-cells proliferate through interaction with macrophages (176), it is logical to think that macrophages are the cells that initiate and direct T-cell response, and that the adaptive ”
Cytokines and chemokines: At the crossroads of cell signalling and inflammatory disease. (2014, background): “This can then lead to the induction of IL-1β expression [7,8].”
An evolving arsenal: viral RNA detection by RIG-I-like receptors (2014, background): “In mammalian cells, pattern recognition receptors (PRRs) protect against host infection by recognizing specific pathogen associated molecular patterns (PAMPs) and eliciting signals that initiate an immune response [1] [2] [3] [4] .”