Gosset Anti-inflammatory effect through immune system regulation Overview
"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.
Mechanism of Action
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
Biological Functions
Disease Associations
Safety Considerations
- Immunosuppression leading to increased infection risk
- Rebound inflammation or loss of immune tolerance
- Organ toxicity (e.g., hepatic, renal, or cardiovascular risks, depending on drug class)
- Cytokine-related adverse events
Interacting Drugs
Associated Biomarkers
| Biomarker |
|---|
| Serum cytokine levels (e.g., IL-10, IL-6, TNF-α) |
| Regulatory T cell (Treg) frequency and function |
| Acute-phase reactants (CRP, ESR) |
| Disease-specific markers (as relevant to the underlying pathology) |