Single nuclei RNA sequencing of mouse dorsal root, nodose, and trigeminal ganglia from humanized JAK1 gain-of-function mice

Janus kinase 1 (JAK1) critically mediates downstream signaling from a variety of immune receptors. Gain-of-function mutations in JAK1 in humans lead to immune dysregulation and exaggerated type 2 immune responses, including atopic dermatitis. We have previously shown that JAK1 expressed in neurons mediates cytokine-enhanced itch signaling in atopic dermatitis. We generated a novel mouse expressing human JAK1 with the gain-of-function mutation p.A634D. To better understand how enhanced JAK1 signaling my impact sensory neurons, we performed single nuclei RNA sequencing on different sensory ganglia from JAK1 gain-of-function mice and littermate controls.