Polysaccharide-K-activated immune cell modulation (PSK-immune modulation)

Polysaccharide-K ("PSK", also known as krestin) is an immunomodulatory protein-bound polysaccharide extracted from the mushroom Trametes versicolor ("Coriolus versicolor"). It consists mainly of β-glucans with protein components. Unlike classical drug targets that are individual proteins or genes, PSK acts through multiple mechanisms—primarily by stimulating both innate and adaptive arms of the immune system. It binds various pattern recognition receptors on monocytes/macrophages/dendritic cells—including Toll-like receptors—and triggers downstream signaling pathways that result in increased cytokine production and enhanced activity of T-cells, B-cells, natural killer cells (NK), dendritic cells (DCs), and macrophages. This leads to improved antitumor immunity through both direct effects on tumor growth/apoptosis inhibition/metastasis suppression, indirect effects via enhanced host immunity, correction of chemotherapy-induced immunosuppression, and possible synergy with other anticancer agents. In Japan it has been approved for use alongside conventional cancer therapies. However—as this entry refers broadly to "immune system modulation via polysaccharopeptide/polysaccharide-K activation," it does not represent one discrete molecular entity suitable for classification under standard therapeutic targets like "receptor," "enzyme," etc., but rather describes the pleiotropic actions resulting from administration of these complex natural products. If you need information about specific *receptors* involved in this process—such as Toll-like receptor 4—or wish to focus only on one defined component within this pathway for structured data purposes please specify further.

Other names

Polysaccharide KPSKKrestinCoriolus versicolor polysaccharopeptideMushroom β-glucan

As an agent: - Activates innate and adaptive immune responses by binding to pattern recognition receptors on immune cells such as Toll-like receptors (TLRs), Dectin‑1, mannose receptor (MR), and complement receptor 3 (CR3). - Enhances cytokine secretion from T-cells and macrophages including IL‑2, IFN‑γ, IL‑4. - Promotes maturation/activation of dendritic cells leading to increased antigen presentation. - Increases NK cell cytotoxicity and corrects Th1/Th2 imbalance. - Offsets immunosuppression induced by tumors or cancer therapies.