Exposing mice to a chemical called calcipotriol leads to itching and scratching behavior similar to that observed in humans with atopic dermatitis. Walsh et al. observed prominent infiltration by immune cells called neutrophils at the site where the calcipotriol had been administered during both acute (early) itch and chronic (late) itch. In the acute phase (left) neutrophils led to the production of the cytokine CXCL10, which signals through the receptor CXCR3 to drive itch. CXCR3 is a receptor expressed on the surface of sensory neurons in the skin called nociceptors. In the chronic phase (right), a cytokine called TSLP (not shown) acts with neutrophils to cause itch. The presence of TSLP leads to infiltration by other immune cells (including basophils, eosinophils and mast cells) that are known to contribute to itch. The presence of TSLP also leads to the production of IL-4, which binds to the IL-4 receptors (IL-4R) on nociceptive neurons, making these neurons more likely to respond to histamine and other signals that cause itch.