Anti-inflammatory effect through immune system regulation

"Anti-inflammatory effect through immune system regulation" refers to a therapeutic mechanism involving modulation or suppression of the immune response to reduce inflammation. This effect can be achieved via multiple molecular targets, such as inhibition of pro-inflammatory cytokines (e.g., TNF, IL-1, IL-6), upregulation of anti-inflammatory mediators (e.g., IL-10, IL-4, regulatory T cells), or through immunometabolic reprogramming of immune effector cells. Many approved drugs work through these mechanisms by targeting specific cytokines, cell populations, or signaling/transcriptional pathways that collectively control immune activation and the inflammatory cascade[1][2][3][4][5][7]. Because this term describes a collection of mechanisms and pathways—not a single protein or gene—it is not considered a discrete therapeutic target, and should be replaced with a specific molecular entity (e.g., "Interleukin-6 receptor", "Tumor necrosis factor", or "Glucocorticoid receptor") in structured data.

Other names

Immune regulationImmune modulation for anti-inflammationImmunomodulation (anti-inflammatory)Anti-inflammatory immune mechanism

Inhibition of pro-inflammatory cytokine production (e.g., TNF, IL-6, IL-1β inhibition); Promotion of anti-inflammatory cytokines (e.g., IL-10, IL-4, IL-13 induction); Modulation of immune cell metabolism (e.g., glycolysis inhibition); Stimulation of regulatory T cells (Treg) or other tolerogenic cells; Blockade or stimulation of cytokine receptors