017 Unraveling the kinetics and cellular contributions in type 2 immune responses in atopic dermatitis

Atopic dermatitis (AD) is a chronic inflammatory skin disease associated with barrier defects and microbial dysbiosis. The development progression of AD critically depends on the action type 2 immune cells mediators. However, identity these as well their chronological appearance in establishment are still elusive. This project aims to disclose kinetics cellular contributors responses AD, focusing dynamics interleukin (IL)-4 induction during inflammation pre-clinical models. To mimic impairment, mice were subjected repeated tape stripping (TS) shaved back skin. Medium containing Staphylococcus aureus (S. aureus) was applied induce Both conditions induced either alone or combination at defined time points. Using IL-4 reporter mice, we found that TS S. increased IL-4-producing cell types such T helper cells, basophils natural killer skin, accompanied by mRNA expression IL-13, IL-4, CCL17 CCL22, 6 days after treatment. Skin-draining lymph nodes mimicked previously described IL-4- producing types. Moreover, IL-33, CXCL1 IL-6 detected early points, downregulation barrier-forming proteins within combined treatment aureus. Analyses microbiome WT affirm this finding pointing shift homeostasis characterized predominance Staphylococci TS. shows impairment dysbiosis act synergistically specific types, other features AD. In long term, will clarify role different cytokine- beyond Th2 develop new strategies.