Cited by 170Immune Response and InflammationInflammasome and immune disordersNF-κB Signaling Pathways

Restraint of inflammatory signaling by interdependent strata of negative regulatory pathways

Open access
Murray, Peter J, Smale, Stephen T·2012·Nature Immunology

Abstract

Activation of Toll-like receptor (TLR) signaling and related pathways by microbial products drives inflammatory responses, host-defense pathways and adaptive immunity. The cost of excessive inflammation is cell and tissue damage, an underlying cause of many acute and chronic diseases. Coincident with activation of TLR signaling, a plethora of anti-inflammatory pathways and mechanisms begin to modulate inflammation until tissue repair is complete. Whereas most studies have focused on the signaling components immediately downstream of the TLRs, this Review summarizes the different levels of anti-inflammatory pathways that have evolved to abate TLR signaling and how they are integrated to prevent cell and tissue destruction.

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Crossref · 10.1038/ni.2391

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  • Expression of the M1 phenotype is regulated by transcription factors such as NF-κB, IRF-3, and IRF-5.

    “Expression of the M1 phenotype is regulated by transcription factors such as NF-κB, IRF-3, and IRF-5 [189,190,191].”

    From MicroRNAs as Regulators of Phagocytosis (2022) · cites this paper as [189]

    The “Stratum 5: transcriptional regulation” and “Transcriptional repression of inflammation” sections identify NF-κB as a factor involved in inflammatory gene transcription in macrophages (page not provided). They do not identify IRF-3 or IRF-5 as regulators of the M1 phenotype; the transcriptional-repression section instead mentions IRF4. (LLM, conf=0.84)

    Experimental — accuracy not yet measured
  • Treatment of rats, mice, and pigs with GHK effectively activates systemic healing throughout the animal.

    “The treatment of rats, mice, and pigs with GHK was shown to effectively activate systemic healing throughout the animal.”

    From GHK and DNA: Resetting the human genome to health (2014) · cites this paper as [41]

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Authors
Murray, P. J., & Smale, S. T.
Affiliations
  • St. Jude Children's Research Hospital (US)
  • University of California, Los Angeles (US)
Corresponding author
Murray, Peter J
Venue
Nature Immunology
Published
2012-09-18
Volume
13
Issue
10
Pages
916-924
ISSN
  • 1529-2908 (ISSN-L)
  • 1529-2916
OpenAlex
W2006283298
Cited by
170
References
120
Citations by year
2026: 8 · 2025: 10 · 2024: 4 · 2023: 5 · 2022: 14 · 2021: 10 · 2020: 7 · 2019: 8 · 2018: 8 · 2017: 13 · 2016: 17 · 2015: 19 · 2014: 19 · 2013: 24 · 2012: 4
FWCI
1.95
Type
journal article
Language
en
Open access
Locations
  • Nature Immunology (publishedVersion)
  • PubMed (publishedVersion)
  • Europe PMC (PubMed Central) (acceptedVersion)
  • PubMed Central (acceptedVersion)
Funders
  • Hartwell Foundation
  • National Cancer Institute (P 30CA 21765, R01CA127279, P30CA021765)
  • National Institute of General Medical Sciences (R01GM086372)
  • National Institute of Allergy and Infectious Diseases (R01AI073868)
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 › Biochemistry, Genetics and Molecular Biology › Cancer Research › NF-κB Signaling Pathways
Keywords
Toll-like receptor signaling, anti-inflammatory pathways, negative regulation of inflammation, inflammatory signaling, host defense, tissue damage, tissue repair, innate immunity, adaptive immunity, microbial products
MeSH terms
Animals, Humans, Inflammation, Lipopolysaccharides, Transcription, Genetic, Wound Healing, Signal Transduction, Interleukin-10, Toll-Like Receptors

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