浆细胞样树突状细胞的免疫调控机制与靶向治疗研究进展OA

Under physiological conditions,plasmacytoid dendritic cells(pDCs)exhibit high functional plasticity,enabling a dynamic transition between type Ⅰ interferon secretion and antigen presentation in response to microenvironmental signals.These distinct functional states support early antiviral innate immunity and initiation of adaptive immune responses,respectively.However,dysregulation of this plasticity is closely associated with disease pathogenesis.In autoimmune conditions such as systemic lupus erythe-matosus,pDCs adopt an abnormally activated phenotype characterized by sustained type Ⅰ interferon overproduction,which drives chronic inflammation and autoimmune pathology.Conversely,within tumor microenvironment,antigen-presenting function of pDCs is suppressed,leading to local immune tolerance and promoting tumor immune evasion.This review focuses on physiological basis and pathological disruption of pDCs plasticity,systematically elaborating its regulatory mechanisms,disease relevance,and emerging ther-apeutic strategies.