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Toll-like receptors in the pathogenesis of neuroinflammation
Abstract
Toll-like receptors (TLRs) are discovered as crucial pattern recognition receptors (PRRs) involved in the recognition of pathogen-associated molecular patterns (PAMPs). Later studies showed their involvement in the recognition of various damage/danger-associated molecular patterns (DAMPs) generated by host itself. Thus, TLRs are capable of recognizing wide-array of patterns/molecules derived from pathogens and host as well and initiating a proinflammatory immune response through the activation of NF-κB and other transcription factors causing synthesis of proinflammatory molecules. The process of neuroinflammation is seen under both sterile and infectious inflammatory diseases of the central nervous system (CNS) and may lead to the development of neurodegeneration. The present article is designed to highlight the importance of TLRs in the pathogenesis of neuroinflammation under diverse conditions. TLRs are expressed by various immune cells present in CNS along with neurons. However out of thirteen TLRs described in mammals, some are present and active in these cells, while some are absent and are described in detail in main text. The role of various immune cells present in the brain and their role in the pathogenesis of neuroinflammation depending on the type of TLR expressed is described. Thereafter the role of TLRs in bacterial meningitis, viral encephalitis, stroke, Alzheimer's disease (AD), Parkinson's disease (PD), and autoimmune disease including multiple sclerosis (MS) is described. The article is designed for both neuroscientists needing information regarding TLRs in neuroinflammation and TLR biologists or immunologists interested in neuroinflammation.
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“Several of them, especially TLR2, 4, and 9, have vital contributions to the development of neurodegenerative diseases.276”
From Role of neuroinflammation in neurodegeneration development (2023) · cites this paper as [276]
In the citing paper
“TLR activation leads to receptor dimerization and the recruitment of adapter proteins, such as Toll/interleukin 1 receptor (TIR) domain-containing adapter interferon-β (TRIF) and myeloid differentiation primary-response protein 88 (MyD88)276”
From Role of neuroinflammation in neurodegeneration development (2023) · cites this paper as [276]
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Metadata
- Authors
- Kumar, V.
- Affiliations
- The University of Queensland (AU)
- Corresponding author
- Kumar, V.
- ORCID
- Kumar, V.
- Venue
- Journal of Neuroimmunology
- Publisher
- Elsevier BV
- Published
- 2019-07
- Volume
- 332
- Pages
- 16-30
- ISSN
- 0165-5728 (ISSN-L)
- OpenAlex
- W2924166680
- Cited by
- 331
- References
- 255
- Citations by year
- 2026: 25 · 2025: 41 · 2024: 50 · 2023: 55 · 2022: 61 · 2021: 47 · 2020: 46 · 2019: 6
- FWCI
- 4.18
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Journal of Neuroimmunology (publishedVersion)
- PubMed (publishedVersion)
- 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, neuroinflammation, pattern recognition receptors, damage-associated molecular patterns, NF-κB signaling, inflammatory cytokines, neurodegeneration, bacterial meningitis, viral encephalitis, stroke, Alzheimer's disease, Parkinson's disease, multiple sclerosis
- MeSH terms
- Alarmins, Pathogen-Associated Molecular Pattern Molecules, Animals, Astrocytes, Brain, Brain Diseases, Cerebrovascular Disorders, Encephalitis, Humans, Meningitis, Neurons, Oligodendroglia, Neuroimmunomodulation, Signal Transduction, Microglia, Neurodegenerative Diseases, Receptors, Pattern Recognition, Toll-Like Receptors, Myeloid Differentiation Factor 88
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