IL-23R Tg mice overexpress interleukin 23 receptor (Il23r) cDNA, amplified from a T helper (Th) 17 cell pool, in T cells under control of the human CD2 promoter. IL-23R Homozygotes are viable and fertile. IL-23R is the receptor for the cytokine, IL-23, which is primarily secreted by activated dendritic cells, monocytes, and macrophages, and functions in innate and adaptive immunity. It has been shown to be important in some inflammatory diseases including experimental autoimmune encephalitis, collagen-induced arthritis, and intestinal inflammation, as well as tumorigenesis. Mutations in IL-23R are an important susceptibility factor for these disorders. IL-23R Tg mice exhibit increased airway infiltration of eosinophils and T helper (Th) 2 cytokine production, including IL-4, IL-5, and IL-13. IL-23 signaling regulates allergic asthma through modulation of Th2 cell differentiation.

IL-23R Tg mice overexpress IL-23R in T cells. In an allergen-induced asthma model,
mice exhibit increased airway infiltration of eosinophils and T helper 2 cytokine production. These transgenics mice may be useful in studies related to inflammatory diseases.

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