Epithelial Cell Death and Inflammation in Skin

  • Snehlata Kumari
  • Manolis Pasparakis
Part of the Current Topics in Microbiology and Immunology book series (CT MICROBIOLOGY, volume 403)


The presence of dying cells in inflamed tissues has been recognized since many years, but until recently cell death was considered primarily a consequence of inflammation. Recent data in mouse models suggest that cell death could provide a potent trigger of inflammation. The identification of necroptosis as a new type of regulated necrotic cell death that is induced by death receptors, toll like receptors and type I interferon receptor indicated that necroptosis could contribute to the proinflammatory properties of these receptors. This is particularly relevant to the skin, a tissue that provides a life-sustaining structural and immunological barrier with the environment and is constantly exposed to mechanical, chemical, and microbial insults. Studies in mouse models showed that sensitization of keratinocytes to apoptosis or necroptosis triggered by TNF and other stimuli causes severe chronic inflammatory skin lesions. In addition, keratinocyte death is a prominent histopathological feature of many inflammatory skin diseases, suggesting that death of epithelial cells could contribute to the pathogenesis of skin inflammation . Here we review recent studies in genetic mouse models providing evidence that keratinocyte death is a potent trigger of skin inflammation and discuss their potential relevance for human inflammatory skin diseases.


Skin Inflammation Inflammatory Skin Disease Epidermal Hyperplasia Incontinentia Pigmenti TNFR1 Signaling 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.



Research in the authors’ laboratory is funded by the ERC (2012-ADG_20120314), the DFG (SFB670, SFB829, SPP1656), the European Commission [Grants 223404 (Masterswitch) and 223151 (InflaCare)], the Deutsche Krebshilfe, the Else Kröner-Fresenius-Stiftung and the Helmholtz Alliance (PCCC).


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Copyright information

© Springer International Publishing Switzerland 2015

Authors and Affiliations

  1. 1.Institute for GeneticsUniversity of CologneCologneGermany
  2. 2.Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD)University of CologneCologneGermany
  3. 3.Center for Molecular Medicine (CMMC)University of CologneCologneGermany

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