Cited by 2,738Immune Response and InflammationNF-κB Signaling PathwaysInflammation biomarkers and pathways

Points of control in inflammation

Nathan, Carl·2002·Nature

Abstract

Inflammation is a complex set of interactions among soluble factors and cells that can arise in any tissue in response to traumatic, infectious, post-ischaemic, toxic or autoimmune injury. The process normally leads to recovery from infection and to healing, However, if targeted destruction and assisted repair are not properly phased, inflammation can lead to persistent tissue damage by leukocytes, lymphocytes or collagen. Inflammation may be considered in terms of its checkpoints, where binary or higher-order signals drive each commitment to escalate, go signals trigger stop signals, and molecules responsible for mediating the inflammatory response also suppress it, depending on timing and context. The non-inflammatory state does not arise passively from an absence of inflammatory stimuli; rather, maintenance of health requires the positive actions of specific gene products to suppress reactions to potentially inflammatory stimuli that do not warrant a full response.

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Crossref · 10.1038/nature01320

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  • Without sufficient glucocorticoid regulation, the duration and/or intensity of the inflammatory response increases, heightening risk for acute exacerbations such as occur in asthma and autoimmune diseases, as well as for the onset and progression of chronic inflammatory diseases such as CVD and type II diabetes.

    “Without sufficient glucocorticoid regulation, the duration and/or intensity of the inflammatory response increases, heightening risk for acute exacerbations such as occur in asthma and autoimmune diseases, as well as for the onset and progression of chronic inflammatory diseases such as CVD, and type II diabetes (12).”
  • Many endogenous antiinflammatory mediators can prevent cytokine-mediated disease.

    “Many endogenous antiinflammatory mediators can prevent cytokine-mediated disease (reviewed in ref. 10).”
  • When sufficient concentrations of endogenous antiinflammatory mediators are achieved, proinflammatory cytokine levels are inhibited, the inflammatory response is dampened, and damage is prevented.

    “When sufficient concentrations are achieved, proinflammatory cytokine levels are inhibited, the magnitude of the inflammatory response is dampened, and damage is prevented.”
  • High cellular ROS levels are associated with cancer, diabetes, inflammatory diseases, ischemia-related diseases, and neurodegeneration.

    “Second, high cellular ROS levels are associated with cancer, diabetes, inflammatory diseases, ischemia-related diseases, and neurodegeneration, and are thus commonly thought to contribute to human pathologies and aging 80–83.”

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Authors
Nathan, C.
Affiliations
Cornell University (US)
Corresponding author
Nathan, Carl
Venue
Nature
Published
2002-12
Volume
420
Issue
6917
Pages
846-852
ISSN
  • 0028-0836 (ISSN-L)
  • 1476-4687
OpenAlex
W2056879548
Cited by
2,738
References
115
Citations by year
2026: 72 · 2025: 86 · 2024: 117 · 2023: 122 · 2022: 156 · 2021: 141 · 2020: 112 · 2019: 109 · 2018: 113 · 2017: 134 · 2016: 114 · 2015: 128 · 2014: 145 · 2013: 143 · 2012: 128
FWCI
5.29
Type
journal article
Language
en
Open access
closed
Locations
  • Nature (publishedVersion)
  • PubMed (publishedVersion)
  • RePEc: Research Papers in Economics (submittedVersion)
Funders
  • Hearst Foundations
  • National Institutes of Health
Topics
  • Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › NF-κB Signaling Pathways
  • Life Sciences › Immunology and Microbiology › Immunology › Inflammation biomarkers and pathways
Keywords
inflammation, inflammatory signaling, anti-inflammatory regulation, tissue damage, leukocytes, lymphocytes, collagen, immune regulation
MeSH terms
Animals, Humans, Inflammation, Cytokines, Apoptosis, Oxidative Stress, Genetic Predisposition to Disease

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