Abstract
Toll-like receptors (TLRs) are a family of well-known pathogen recognition receptors practical on immune cells and critical for the host defense during infections. They recognize various types of immunostimulatory components from microorganisms, such as lipids, nucleic acids, and proteins. The ligand-loaded TLRs form homotypic or heterotypic dimers to transduce their signal to cytosolic adaptor molecules, MyD88, and/or TRIF. Their signal transductions are initiated on specialized subcellular compartments, called “activation platform” by recruitment of signaling molecules. The activation platforms are regulated by membrane anchoring sorting adaptor molecules like TIRAP and TRAM. Activated TLRs induce productions of proinflammatory cytokines and type I interferons via triggering transcription factors, like NFκB, AP-1, and IRFs. Acquired immune reactions are also accelerated by the induction of co-stimulatory molecules and antigen loading on major histocompatibility complex (MHC) by the consequence of TLRs’ responses. On the other hand, TLRs have another aspect on autoimmune diseases by the disorder of self-derived TLRs’ ligands.
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Tanimura, N., Miyake, K. (2014). Toll-Like Receptors. In: Endo, T., Seeberger, P., Hart, G., Wong, CH., Taniguchi, N. (eds) Glycoscience: Biology and Medicine. Springer, Tokyo. https://doi.org/10.1007/978-4-431-54836-2_142-1
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DOI: https://doi.org/10.1007/978-4-431-54836-2_142-1
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Publisher Name: Springer, Tokyo
Online ISBN: 978-4-431-54836-2
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