The increasing prevalence of chronic autoimmune-mediated inflammatory diseases (AIMIDs) in ageing western societies is a major challenge for the drug development industry. The current high medical need for more-effective treatments is at least in part caused by our limited understanding of the mechanisms that drive chronic inflammation. Here, we postulate a role for immunosenescence in the progression of acute to chronic inflammation via a dysregulated response to primary injury at the level of the damaged target organ. A corollary to this notion is that treatment of acute versus chronic phases of disease might require differential targeting strategies.
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