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The immune-inflammatory reaction is not a single molecule or receptor but rather a complex biological process that occurs in response to tissue injury or infection. It involves coordinated actions of various immune cells, blood vessels, signaling molecules like cytokines and chemokines, and molecular mediators. The main purpose is to eliminate harmful stimuli such as pathogens or damaged cells and initiate tissue repair. The classic signs are heat (*calor*), redness (*rubor*), swelling (*tumor*), pain (*dolor*), and loss of function (*functio laesa*). This process is mediated by both innate immunity mechanisms—such as activation via Toll-like receptors—and adaptive immunity components like B cells and T cells. Dysregulation can lead to chronic inflammation or autoimmune diseases. Drugs targeting this process typically act on key enzymes involved in inflammatory mediator synthesis or suppress the activity of pro-inflammatory cytokines.[4][3][5]
Inhibition of cyclooxygenase enzymes by NSAIDs reduces production of prostaglandins and other inflammatory mediators[1] Suppression of cytokine production by corticosteroids and immunosuppressants[2]
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