Abstract
Atopic dermatitis (AD) is a chronic inflammatory skin disease associated with barrier defects and dysbiosis. The development and progression of AD critically depends on the action of type 2 immune cells and mediators, whose identity and chronological appearance in the establishment of AD are still elusive. We aim to disclose the kinetics and cellular contributors of type 2 immune responses in AD, focusing on the dynamics of interleukin (IL)-4 induction during skin inflammation in pre-clinical models.
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