IκBζ-deficient epidermis mediates systemic autoimmune inflammation via skin dysbiosis.

Skin microbiota affect systemic inflammation through mechanisms that have not been completely elucidated. We previously demonstrated that keratinocyte-specific IκBζ-deficient mice spontaneously develop autoimmune inflammation resembling human Sjögren syndrome. In this study, we examined how IκBζ-deficient epidermis dictates systemic autoimmune inflammation onset. To examine if IκBζ-deficient keratinocytes are susceptible to apoptotic stimuli in a steady state, we performed microarray analysis of untreated murine back epidermis. Data indicate that IκBζ-deficient epidermis is susceptible to environment antigens through apoptosis-related gene upregulation Gene expression in epidermis obtained from Nfkbiz flox/flox mouse and Nfkbiz flox/flox; K5-cre mouse. In Nfkbiz flox/flox; K5-cre mouse, IκBζ is deficient in the epidermis under the control of keratin 5 promoter.