Abstract
IKK/NF-kB signalling controls inflammation and cell death and is important to maintain tissue homeostasis. Keratinocyte-specific deletion of IKK2 (IKK2E-KO) leads to TNFR1-dependent skin inflammation in mice. IKK2E-KO mice showed increased numbers of apoptotic and necrotic keratinocytes, and upregulation of inflammatory cytokines mediators in the epidermis. We proposed that keratinocyte death could trigger inflammation. Receptor Interacting Protein Kinase (RIPK1) induces cell death via kinase activity-dependent functions.
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