Recognition and signaling by toll-like receptors.

By A. West, A. A. Koblansky, S. Ghosh. Annual Review of Cell and Developmental Biology, 2006

758 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/fe724d7622cab0a7a73ca8ed4baaf7116f5ab8ed

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Citations in the corpus

Inflammasomes and their roles in health and disease. (2012, background): “However, K+ and other ion fluxes also have been implicated in activation of the Nlrp1b (Ali et al. 2011, Fink et al. 2008, Newman et al. 2009, Wickliffe et al. 2008) and Nlrc4 inflammasomes (Arlehamn et al. 2010).”
NF-κB in the liver—linking injury, fibrosis and hepatocellular carcinoma (2011, background): “Among the most potent activators of NF-κB are pathogen-derived molecules (such as lipopolysaccharide [LPS], viral and bacterial DNA and RNA) that stimulate Toll-like receptors (TLRs), as well as inflammatory cytokines such as tumor necrosis factor (TNF) or interleukin (IL)-1”
Pathophysiology of Cisplatin-Induced Acute Kidney Injury (2014, background): “TLRs have various functions as an important component of innate immune system by recognizing pathogenassociated molecular patterns and also endogenous signals of tissue injury [97].”
Mitochondria in innate immune responses (2011, background): “The list of PRRs known to sense PAMPs is extensive, and is comprised most notably of four families: Toll-like receptors (TLRs), nucleotide oligomerization domain (NOD)-like receptors (NLRs), C-type lectin receptors (CLRs) and retinoic acid-inducible gene I (RIG-I)-like receptors (RLRs”
A New Mesenchymal Stem Cell (MSC) Paradigm: Polarization into a Pro-Inflammatory MSC1 or an Immunosuppressive MSC2 Phenotype (2010, background): “Toll-like receptors recognize “danger” signals and their activation leads to profound cellular and systemic responses that mobilize innate and adaptive host immune cells [16]– [20].”
The Role of TLR2 in Infection and Immunity (2012, background): “A cascade of events occurs following PAMP recognition by PRRs, which activate host defense mechanisms to prevent or fight off infections and initiate and enhance a subsequent adaptive immune response (West et al., 2006).”
Inhibiting NF-κB Activation by Small Molecules As a Therapeutic Strategy (2010, neutral): “Recruitment of these adaptors leads to sequential activation of IRAK1/2 and IKK and eventual release of active NF-κB [211].”