特应性皮炎中肥大细胞介导的神经免疫对话研究新视角OA

Atopic dermatitis(AD)is an inflammatory skin disease characterized by chronic pruritus,epidermal barrier dysfunction,and immune dysregulation.Its pathogenesis is closely associated with neuro-immune interactions.Mast cells(MCs)are key effector cells that are anatomically adjacent to sensory nerve endings and drive the vicious cycle of"pruritus-inflammation-barrier damage"through bidirectional signaling pathways.MCs release mediators such as histamine and interleukin-31(IL-31),which activate transient re-ceptor potential vanilloid 1(TRPV1)-expressing neurons to transmit pruritic signals.Conversely,neuropep-tides secreted by sensory neurons,including substance P and calcitonin gene-related peptide(CGRP),in-duce MC degranulation via their surface receptors,thereby forming a positive feedback loop.This article reviews several typical neuromediators and their corresponding receptors on MCs,with a focus on the activation of intra-cellular signaling pathways and the subsequent release of inflammatory mediators.Furthermore,it discusses the mechanisms by which these interactions contribute to immune dysregulation in AD,aiming to provide new per-spectives and potential strategies for the clinical treatment of AD.