Toll-like Receptors and the control of immunity
By Katherine A. Fitzgerald, Jonathan C. Kagan. Cell, 2020
1,813 citations recorded by the source corpus.
Summary The study of innate immunity and its link to inflammation and host defenses encompasses diverse areas of biology, ranging from genetics and biophysics to signal transduction and physiology. Central to our understanding of these events are the Toll-like Receptors (TLRs), an evolutionarily ancient family of pattern recognition receptors. Herein, we describe the mechanisms and consequences of TLR-mediated signal transduction, with a focus on themes identified in the TLR pathways that also explain the operation of other immune signaling pathways. These themes include the detection of conserved microbial structures to identify infectious agents and the use of supramolecular organizing centers (SMOCs) as signaling organelles that ensure digital cellular responses. Further themes include mechanisms of inducible gene expression, the coordination of gene regulation and metabolism, and the influence of these activities on adaptive immunity. Studies in these areas have informed the development of next-generation therapeutics, thus ensuring a bright future for research in this area.
Subfields: Immunology
View Paper: https://www.semanticscholar.org/paper/0e963990263d8bad3f1d1c8d6070dbeaa08902b9
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In Immunology
Citations in the corpus
- TLR4 and CD14 trafficking and its influence on LPS-induced pro-inflammatory signaling (2020, background): “The initiation of the adaptive immune responses follows activation of various TLRs and involves antigen presentation in the context of major histocompatibility complex (MHC) class I and II, as reviewed by [5, 117].”
- Pattern recognition receptors in health and diseases (2021, background): “Innate immune cells produce different types of cytokines through signal transduction initiated after PRRs recognize PAMPs, which directly affect the differentiation of T helper type 1 (Th1), Th2, Th17, and other subgroups in adaptive immunity.(15) For example, pathogenic microorganisms activate macr”