The role of pattern-recognition receptors in innate immunity: update on Toll-like receptors
Abstract
The discovery of Toll-like receptors (TLRs) as components that recognize conserved structures in pathogens has greatly advanced understanding of how the body senses pathogen invasion, triggers innate immune responses and primes antigen-specific adaptive immunity. Although TLRs are critical for host defense, it has become apparent that loss of negative regulation of TLR signaling, as well as recognition of self molecules by TLRs, are strongly associated with the pathogenesis of inflammatory and autoimmune diseases. Furthermore, it is now clear that the interaction between TLRs and recently identified cytosolic innate immune sensors is crucial for mounting effective immune responses. Here we describe the recent advances that have been made by research into the role of TLR biology in host defense and disease.
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The adaptive immune system can recognize mitochondria.
“The adaptive immune system can also recognize mitochondria. This concept is important, as the immune response initiated by mitochondrial DAMPs may be different if the adaptive immune system is also implicated32,33.”
From Anti-mitochondrial autoantibodies in systemic lupus erythematosus and their association with disease manifestations (2019) · cites this paper as [32]
For the initial detection of microbes, the immune system utilizes pattern-recognition receptors such as TLRs to activate MyD88-dependent signaling and ultimately activate NF-κB.
“For the initial detection of microbes, the immune system utilizes pattern-recognition receptors (PRRs), such as TLRs to activate MyD88-dependent signaling and ultimately activate NF-κB (324).”
From IL-6 in inflammation, autoimmunity and cancer (2021) · cites this paper as [324]
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“Interestingly, TLR signaling, in particular TLR2 and TLR4, has been co-opted by endogenous signaling molecules which are thought to alert microglia to a variety of internal conditions such as cellular stress, damage or death (Kawai and Akira, 2010).”
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- Authors
- Kawai, T., & Akira, S.
- Affiliations
- Immunology Frontier Research Center, The University of Osaka (JP)
- Corresponding author
- Akira, Shizuo
- Venue
- Nature Immunology
- Published
- 2010-04-20
- Volume
- 11
- Issue
- 5
- Pages
- 373-384
- ISSN
- 1529-2908 (ISSN-L)
- 1529-2916
- OpenAlex
- W2109491705
- Cited by
- 9,304
- References
- 13
- Citations by year
- 2026: 553 · 2025: 545 · 2024: 542 · 2023: 525 · 2022: 554 · 2021: 661 · 2020: 654 · 2019: 622 · 2018: 558 · 2017: 568 · 2016: 611 · 2015: 588 · 2014: 622 · 2013: 575 · 2012: 568
- FWCI
- 42.97
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- Locations
- Nature Immunology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Ministry of Education, Culture, Sports, Science and Technology
- National Institutes of Health (AI070167)
- National Institute of Allergy and Infectious Diseases (P01AI070167)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Inflammasome and immune disorders
- Life Sciences › Immunology and Microbiology › Immunology › Immunotherapy and Immune Responses
- Keywords
- Toll-like receptors, pattern recognition receptors, innate immunity, host defense, autoimmunity, inflammatory diseases, pathogen recognition
- MeSH terms
- Animals, Autoimmune Diseases, Humans, Immunity, Innate, Nucleic Acids, Nucleoproteins, Signal Transduction, Toll-Like Receptors, Host-Pathogen Interactions, Adaptive Immunity
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