Trained immunity

Trained immunity refers to a non-classical, memory-like property of the innate immune system, distinguished by long-term epigenetic and metabolic reprogramming of innate immune cells (such as monocytes, macrophages, natural killer cells, and progenitor cells). Unlike adaptive immunity, which requires antigen-specific lymphocyte memory, trained immunity confers a broadly enhanced response to subsequent and even unrelated infections and threats by enabling these cells to express higher levels of pro-inflammatory cytokines and effector functions on re-stimulation. Mechanistically, it is induced by both infectious (pathogen-associated molecular patterns like BCG and β-glucan) and sterile (damage-associated molecular patterns, cytokines) stimuli, acting via pattern recognition receptors (e.g., dectin-1, IL-1R, NOD2), metabolic regulators (mTOR, glycolysis), and epigenetic modifiers (histone methylation/acetylation). The process is implicated in protective immunity against infection, but excessive or dysregulated trained immunity can contribute to pathological inflammation, autoimmunity, and transplant rejection. Interventions may aim to induce or suppress trained immunity therapeutically, most commonly via vaccines, immune modulators, metabolic inhibitors, or epigenetic therapies. In summary, "Trained immunity" is a process and biological phenomenon, not a molecular target. It should not be listed as a therapeutic target molecule or receptor for structured databases focused on canonical targets.

Other names

Innate immune memory

Induction by epigenetic and metabolic reprogramming (pro-inflammatory state via histone modification and altered metabolism in innate immune cells) Suppression by inhibition of receptor signaling (e.g., IL-1 receptor, dectin-1, NOD2), mTOR pathway, lipid metabolism