John Libbey Eurotext

European Journal of Dermatology

Apoptotic and necroptotic cell death in cutaneous inflammation Article à paraître

Auteurs
Inserm U976, Equerre Bazin, Hôpital St-Louis, 1 av. Claude Vellefaux, 75475 Paris Cedex 10, France, Université Paris-Diderot, UMR-S 976, Equerre Bazin, Hôpital St-Louis, 1 av. Claude Vellefaux, 75475 Paris Cedex 10, France, Service de dermatologie, Hôpital St-Louis, 1 av. Claude Vellefaux, 75475 Paris Cedex 10, France
  • Mots-clés : apoptosis, necroptosis, keratinocytes, skin inflammation, mouse models
  • DOI : 10.1684/ejd.2013.1977

Epidermal keratinocytes provide an essential structural and immunological barrier forming the first line of defense against potentially pathogenic microorganims. Mechanisms regulating barrier integrity and innate immune responses in the epidermis are important for the maintenance of skin immune homeostasis and the pathogenesis of inflammatory skin diseases. Cell death, and in particular, apoptosis, has been suggested to play a key role in numerous skin inflammatory diseases. Supporting these reports, studies in mouse models have emphasized the role of increased keratinocyte apoptosis in cutaneous inflammation. Necrosis has long been considered as a passive form of cell death, but recent reports have unraveled the molecular regulation of necrosis. Programmed necrosis, also termed necroptosis, has been recently implicated in mouse models of skin inflammation. In this review, we discuss the respective roles of apoptotic or necrotic cell death of epidermal keratinocytes in mouse models of cutaneous inflammation and in the physiopathology of human inflammatory dermatoses.