A sympathetic-basophil axis promotes skin inflammation
As the largest barrier organ of the body, the skin integrates immune and peripheral sensory nervous systems to respond to environmental stimuli. While sensory neuroimmune interactions in the skin are extensively studied, the role of the sympathetic nervous system (SNS) in skin immunity remains unclear. We show that stress exacerbates atopic dermatitis (AD)-like inflammation in murine models by driving basophil infiltration through SNS activation, independent of the hypothalamic-pituitary-adrenal axis.  By elucidating the crosstalk between SNS and inflammation pathways, our study underscores the critical role of autonomic responses in chronic inflammatory skin diseases. Overall design: Following the ablation of tyrosine hydroxylase-positive (TH?) nerves by 6-hydroxydopamine hydrobromide, live CD45? lineage? (CD3e, CD5, CD11c, CD19, NK1.1)  cells of the ear skin of WT mice were sorted by fluorescence-activated cell sorting (FACS) and analyzed using scRNA-seq.