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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I thank L. Grant for introducing me to the study of inflammation, K. F. Austen, P. Bernstein, A. Ding, M. Fuortes and L. Old for critique of the paper and S. Chen for help in the library. It is regretted that space precluded citing many relevant sources. Preparation of this article was supported by NIH. The Department of Microbiology and Immunology acknowledges the support of the William Randolph Hearst Foundation.
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Nathan, C. Points of control in inflammation. Nature 420, 846–852 (2002). https://doi.org/10.1038/nature01320
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