ILC2 Activity in Infants Induces Stronger Eosinophilic Skin Inflammation Than in Adult in an Atopic Dermatitis Mouse Model.

To clarify why the pathogenesis of atopic dermatitis (AD) reportedly differs between infants and adults, we performed in vivo experiments using a mouse model of AD. A vitamin D analogue (calcipotriol; MC903) or vehicle (Ethanol) was topically applied to the ears of C57BL6 wild-type mice at 2 weeks (infant mice) or 9 weeks of age (adult mice). Skin inflammation was evaluated by ear thickness and histology. The immune cell composition of ear tissues was evaluated by flow cytometry. Expression of cytokines was determined by ELISA and quantitative PCR. Ear thickness, the numbers of eosinophils and group 2 innate lymphoid cells (ILC2s), and expression of type 2 cytokines in the ears were each significantly greater in MC903-treated infant mice compared with the adult mice. However, expression of such upstream regulators of inflammation as TSLP and IL-33 showed the opposite tendency. In addition, type 2 cytokine production by ILC2s was significantly higher in infant mice compared to adult mice. T2 inflammation was more severe in infant mice than in adult mice, probably due to the former’s greater ILC2 activity.