神经递质功能分组介导特应性皮炎的神经免疫调控机制研究进展OA

Atopic dermatitis(AD)is a chronic inflammatory skin disease characterized by per-sistent inflammation,intractable pruritus,and skin barrier impairment,in which dysregulation of the neuro-immune-barrier network represents a key pathogenic mechanism.As major regulators of the neuroimmune axis,neurotransmitters can be functionally classified into excitatory,inhibitory,and auxiliary modulatory groups,and their imbalance directly contributes to inflammatory amplifi-cation,itch persistence,and barrier dysfunction in AD.Excitatory neurotransmitters,including norepinephrine/epinephrine,glutamate,and acetylcholine,mainly mediate inflammatory activa-tion and pruritic signal transmission through receptors such as β2-adrenergic receptor(β2AR),glutamate receptor kainate 2(GluK2),and nicotinic acetylcholine receptor(nAChR).Inhibitory neurotransmitters,such as γ-aminobutyric acid and glycine,regulate neural sensitization and maintain itch homeostasis through inhibitory circuits in the spinal dorsal horn.Auxiliary modulato-ry neurotransmitters,including tryptophan,5-hydroxytryptamine,and melatonin,are involved in barrier repair and inflammatory integration via metabolic pathways,circadian regulation,and mi-crobiota-related interactions.Translational evidence indicates that the AhR axis is now entering the stage of clinical therapeutic exploration,while GABA receptors,GluK2,HTR7,and topical me-latonin delivery remain largely at the preclinical stage.This review summarizes the core mecha-nisms and translational implications of functionally distinct neurotransmitter groups in AD,provi-ding a theoretical basis for the development of novel diagnostic and therapeutic strategies targeting the neuroimmune axis.