Anti-inflammatory response

"Anti-inflammatory response" is not a specific molecule, receptor, enzyme, transporter, or other discrete therapeutic target. Instead, it refers to a complex set of biological processes that act to suppress inflammation and restore tissue homeostasis after an immune challenge. This process involves multiple cell types—primarily macrophages—and the release of various mediators including anti-inflammatory cytokines like interleukin 10 (IL‑10), transforming growth factor beta (TGF‑β), lipid mediators such as prostaglandins and lipoxins, annexin I, thrombospondin 1 (TSP‑1), fractalkine, adenosine acting via A2A receptors on macrophages,[1] among others.\n\nThe anti-inflammatory response is essential for preventing excessive tissue damage during infection or injury and for resolving inflammation once the threat has passed.[4] Dysregulation can result in chronic inflammatory conditions. Drugs commonly described as "anti-inflammatories," such as NSAIDs and corticosteroids,[7] work by inhibiting proinflammatory pathways rather than targeting any single "anti-inflammatory" molecule.\n\nBecause "anti-inflammatory response" describes a physiological process rather than an individual molecular entity with defined structure/function relationships suitable for direct drug targeting, it is not considered a canonical therapeutic target. Therefore, entries requiring structured information about specific molecules/receptors should instead focus on well-defined targets involved in this process—such as interleukin 10 receptor or transforming growth factor beta receptor.\n\nIn summary, the term "anti-inflammatory response" is too broad and non-specific to serve as an individual molecular target; it encompasses many molecules working together within the immune system's regulatory network.[1][2][4]

Other names

Anti-inflammatory responseAnti-inflammationInflammatory resolution (context-dependent)

Inhibition of pro-inflammatory cytokine production; Promotion of anti-inflammatory cytokines such as IL‑10 and TGF‑β release by immune cells