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.
Keywords
InflammationInflammatory responseContext (archaeology)ImmunologyTissue repairMedicineNeuroscienceBiologyCell biology
MeSH Terms
AnimalsApoptosisCytokinesGenetic Predisposition to DiseaseHumansInflammationOxidative Stress
Affiliated Institutions
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Publication Info
- Year
- 2002
- Type
- review
- Volume
- 420
- Issue
- 6917
- Pages
- 846-852
- Citations
- 2649
- Access
- Closed
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Cite This
Carl Nathan
(2002).
Points of control in inflammation.
Nature
, 420
(6917)
, 846-852.
https://doi.org/10.1038/nature01320
Identifiers
- DOI
- 10.1038/nature01320
- PMID
- 12490957