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

ABSTRACT: 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

ORGANISM(S): Mus musculus

PROVIDER: GSE165515 | GEO | 2022/08/11

REPOSITORIES: GEO

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

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

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