Abstract
Mutations in filaggrin underlie ichthyosis vulgaris (IV) and contribute to increased risk of Atopic Dermatitis (AD), conditions typified by disruption of skin microbial communities and the cutaneous immune response. Yet, it remains unclear how neonatal skin barrier compromise in the setting of filaggrin deficiency alters the quality of commensal-specific T cells and the role of such responses in heightened skin inflammation. To test this we colonized the skin of neonatal flg-/- pups with a strain of Staphylococcus epidermidis engineered to express the model antigen 2w (S.
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