Disruption of skin barrier function due to filaggrin deficiency and microbial dysbiosis promotes the release of epidermal alarmins, such as interleukin (IL)-33 and thymic stromal lymphopoietin (TSLP) (6, 7); these proinflammatory signals recruit and activate type 2 inflammatory cells (8, 9); local type 2 immune responses further impair the barrier function, thereby facilitating Staphylococcus aureus (S. aureus) colonization or infection (5). Here, TSLP is linked to infection.