Mouse models and in vitro cell culture were used to examine airway expression of the mucosal chemokine CCL28. Low levels of constitutivelyexpressed mRNA were observed in transformed murine epithelial cells, but high levels could be induced by stimulation. Cytokines that signalthrough NF-�B, including IL-1�and TNF-�or via JAK-STAT pathway including oncostatin M induced CCL28 in airway epithelial cells invitro. Immunohistochemistry of murine airway tissue revealed that constitutive expression of CCL28 protein in vivo was low and not ubiquitous.However, abundant expression was detected in epithelia and lymphoid aggregates following allergic sensitization and challenge with ovalbumin.This was accompanied by increased detection of cells expressing CCR10 protein and mRNA in inflamed airways. Taken together, these data supporta role for CCL28 in contributing to allergen driven airway pathologies, show that proinflammatory cytokines can induce this signal and suggest arole for CCR10 expressing cells in airway inflammation.