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Toll-Like Receptors: Sensor Molecules for Detecting Damage to the Nervous System
Abstract
Toll-like receptors (TLRs) are type I transmembrane signaling molecules that are expressed in cells of the innate immune system. In these cells, TLRs function as pattern recognition receptors (PRR) that recognize specific molecular patterns derived from microorganisms. Upon activation, TLRs trigger a cascade of intracellular signaling pathways in innate immune cells, leading to the induction of inflammatory and innate immune responses, which in turn regulate adaptive immune responses. In the nervous system, different members of the TLR family are expressed on glial cells (astrocytes, microglia, oligodendrocytes, and Schwann cells) and neurons. Recently, increasing evidence has supported the idea that TLRs also recognize endogenous molecules that are released from damaged tissue, thereby regulating inflammatory responses and subsequent tissue repair. These findings imply that TLRs on glial cells may also be involved in the inflammatory response to tissue damage in the nervous system. In this review, we discuss recent studies on TLR expression in the cells of the nervous system and their roles in acute neurological disorders involving tissue damage such as strokes, traumatic spinal cord and brain injuries, and peripheral nerve injuries.
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“TLR4 is up-regulated after TBI and recognizes LPSs and endogenous proteins, such as high-mobility group box 1 protein, heat shock proteins, and low-density lipoprotein (132).”
From The anatomy and immunology of vasculature in the central nervous system (2019) · cites this paper as [132]
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Neuroimmunology of Traumatic Brain Injury: Time for a Paradigm Shift
Jassam, Y. N., Izzy, S., Whalen, M., McGavern, D. B., & El Khoury, J. (2017) · Neuron · doi:10.1016/j.neuron.2017.07.010 · Cited by 799
Wang, M., Pan, W., Xu, Y., Zhang, J., Wan, J., & Jiang, H. (2022) · Journal of Inflammation Research · doi:10.2147/jir.s350109 · Cited by 461
“TLR4 is expressed primarily on microglia and sparsely on astrocytes and neurons.(61,62) The binding of TLR4 to appropriate ligands activatesmicroglia, induces a local inflammatory response and promotes the expression of pro-inflammatory cytokines.”
BackgroundMicroglia: Agents of the CNS Pro-Inflammatory Response
Rodríguez-Gómez, J. A., Kavanagh, E., Engskog-Vlachos, P., Engskog, M. K. R., Herrera, A. J., Espinosa-Oliva, A. M., Joseph, B., Hajji, N., Venero, J. L., & Burguillos, M. A. (2020) · Cells · doi:10.3390/cells9071717 · Cited by 365
“3 + ++ Poly(I:C), viral dsRNA [67,74] mRNA from apoptotic cells [75], stathmin[76]”
BackgroundZhu, H., Bian, C., Yuan, J., Chu, W., Xiang, X., Chen, F., Wang, C., Feng, H., & Lin, J. (2014) · Journal of Neuroinflammation · doi:10.1186/1742-2094-11-59 · Cited by 374
“One key factor in secondary brain injury is a complex series of inflammatory responses that is initiated largely through TLRs that possibly interact with endogenous ligands released from damaged cells [32,33].”
BackgroundThe anatomy and immunology of vasculature in the central nervous system
Mastorakos, P., & McGavern, D. (2019) · Science Immunology · doi:10.1126/sciimmunol.aav0492 · Cited by 333
“TLR4 is up-regulated after TBI and recognizes LPSs and endogenous proteins, such as high-mobility group box 1 protein, heat shock proteins, and low-density lipoprotein (132).”
Background
Metadata
- Authors
- Lee, H., Lee, S., Cho, I.-H., & Joong Lee, S.
- Affiliations
- Seoul National University (KR)
- Venue
- Current Protein & Peptide Science
- Publisher
- Bentham Science Publishers Ltd.
- Published
- 2013-03-01
- Volume
- 14
- Issue
- 1
- Pages
- 33-42
- ISSN
- 1389-2037 (ISSN-L)
- OpenAlex
- W2024660851
- Cited by
- 113
- References
- 0
- Citations by year
- 2026: 2 · 2025: 6 · 2024: 3 · 2023: 9 · 2022: 13 · 2021: 4 · 2020: 8 · 2019: 14 · 2018: 8 · 2017: 12 · 2016: 10 · 2015: 13 · 2014: 10 · 2013: 1
- FWCI
- 6.35
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Current Protein and Peptide Science (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Research Foundation of Korea
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Inflammasome and immune disorders
- Keywords
- Toll-like receptors, pattern recognition receptors, innate immunity, nervous system damage, glial cells, astrocytes, microglia, oligodendrocytes, Schwann cells, neuroinflammation, tissue repair, stroke, spinal cord injury, traumatic brain injury, peripheral nerve injury
- MeSH terms
- Animals, Brain Injuries, Humans, Immunity, Innate, Ligands, Neuralgia, Neurons, Spinal Cord Injuries, Signal Transduction, Inflammation Mediators, Stroke, Toll-Like Receptors, Peripheral Nerve Injuries
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