Project description:To better understand the contribution of basophils and fibroblast IL-4 signaling on type 2 skin inflammation, we conducted bulk-RNA seq on from normal and MC903 treated Isotype Cntrl + Mar1 and Il4rafl/fl + Il4raΔPdgfra models respectively.
Project description:To better understand cell-cell interactions driving type 2 skin inflammation, we conducted scRNA-seq on two murine models of type 2 skin inflamation, MC903 and Oxazolone (OXA), using the 10X genomics platform
Project description: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.
Project description: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.
Project description: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.