The history of Toll-like receptors — redefining innate immunity

By Luke A. O'Neill, D. Golenbock, A. Bowie. Nature reviews. Immunology, 2013

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Sepsis: current dogma and new perspectives. (2014, background): “Genetic 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., ”
STING-dependent Cytosolic DNA Sensing Promotes Radiation-induced Type I interferon-dependent Antitumor Immunity in Immunogenic Tumors (2014, background): “…of the adaptor proteins, myeloid differentiation primary-response protein 88 (MyD88), and TIR-domain-containing adaptor protein inducing IFN-b (TRIF), the activation of these four endosomal TLRs leads to significant induction of type I IFN production (Desmet and Ishii, 2012; O’Neill et al., 2013).”
The delivery of therapeutic oligonucleotides (2016, background): “The 10 members of the TLR family in humans primarily respond to ligands that contain pathogen associated molecular patterns derived from bacterial cell walls or membranes and from bacterial or viral nucleic acids (109,110).”
Caspase-8 induces cleavage of gasdermin D to elicit pyroptosis during Yersinia infection (2018, background): “Upon initial pathogen contact with innate immune cells, the host cell signaling through Toll-like receptors (TLRs) simultaneously engages a cell’s intrinsic prosurvival program and produces inflammatory cytokines to propagate the alarm of infection (1).”