Microbial recognition by Toll-like receptors
Abstract
Toll-like receptors (TLRs) sense invasion of microorganisms by detecting microbial components that are conserved among pathogens. Recognition of microbial components by TLRs triggers activation of the innate immune system. Signaling pathways via TLRs originate from conserved cytoplasmic Toll/IL-1 receptor (TIR) domains. Recent accumulating evidence demonstrates that TIR domain-containing adaptors, such as MyD88, TIRAP/Mal, TRIF, and TRAM, regulate TLR-mediated signaling pathways. MyD88 is common to all TLR-mediated pathways, which lead to the production of inflammatory cytokines, whereas TRIF mediates induction of IFN-beta in TLR3 and TLR4 signaling pathways. TIRAP/Mal is implicated in the TLR2- and TLR4-mediated MyD88-dependent signaling pathway. TRAM is specifically involved in the TLR4-mediated TRIF-dependent pathway. Thus, TIR domain-containing adaptors play a pivotal role in TLR signaling pathways, which culminate in pathogen-specific immune responses.
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Epithelial pattern recognition receptors recognize pathogen-associated molecular patterns, of which the TLR family are the most studied, and once activated can recruit inflammatory mediators, cytokine production and chemokine-mediated recruitment of acute inflammatory cells.
“Epithelial pattern recognition receptors recognize molecular patterns unique to bacteria and other microorganisms (pathogen-associated molecular patterns) (Duerkop et al., 2009;Vaishnava et al., 2008) of which the TLR family are the most studied, and once activated can recruit inflammatory mediators, cytokine production and chemokine-mediated recruitment of acute inflammatory cells (Takeda and A”
From The Microbiota-Gut-Brain Axis (2019) · cites this paper as Takeda and Akira, 2004
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- Authors
- Takeda, K., & Akira, S.
- Affiliations
- Research Institute for Microbial Diseases, The University of Osaka (JP)
- Corresponding author
- Akira, Shizuo
- Venue
- Journal of Dermatological Science
- Publisher
- Elsevier BV
- Published
- 2004-04
- Volume
- 34
- Issue
- 2
- Pages
- 73-82
- ISSN
- 0923-1811 (ISSN-L)
- OpenAlex
- W2116766330
- Cited by
- 285
- References
- 92
- Citations by year
- 2026: 5 · 2025: 3 · 2024: 11 · 2023: 7 · 2022: 11 · 2021: 8 · 2020: 6 · 2019: 12 · 2018: 18 · 2017: 8 · 2016: 16 · 2015: 11 · 2014: 13 · 2013: 14 · 2012: 9
- FWCI
- 1.32
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Journal of Dermatological Science (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Japan Research Foundation for Clinical Pharmacology
- Ministry of Education, Culture, Sports, Science and Technology
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Inflammasome and immune disorders
- Health Sciences › Medicine › Infectious Diseases › Tuberculosis Research and Epidemiology
- Keywords
- Toll-like receptors, microbial identification, innate immunity, TIR domain, MyD88, TRIF, tram, TLR signaling pathways, inflammatory cytokines, interferon-beta, TLR3, TLR4, TLR2, pathogen recognition
- MeSH terms
- Animals, Antigens, Differentiation, Bacterial Infections, Humans, Membrane Glycoproteins, Receptors, Cell Surface, Receptors, Immunologic, Signal Transduction, Receptors, Interleukin-1, Adaptor Proteins, Vesicular Transport, Adaptor Proteins, Signal Transducing, Toll-Like Receptors, Toll-Like Receptor 2, Toll-Like Receptor 3, Toll-Like Receptor 4, Myeloid Differentiation Factor 88
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