Sunburned skin activates inflammasomes

Trends Cell Biol. 2008 Jan;18(1):4-8. doi: 10.1016/j.tcb.2007.10.004. Epub 2007 Dec 20.


Ultraviolet (UV) irradiation injures the epidermis, resulting in sunburn and inflammation. UV-irradiated keratinocytes secrete interleukin-1beta through a caspase-1-dependent mechanism. In seeking a link between UV-irradiation and caspase-1 activation, a prominent role for the NOD-like receptor (NLR) family of innate immunity proteins was discovered recently. NLRs activate caspases through the assembly of macromolecular complexes called 'inflammasomes.' Although the mechanism by which UV-irradiation activates inflammasomes remains obscure, these recent findings shed light on NLRs as intermediaries between cell injury and inflammation.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Caspase 1 / metabolism*
  • Enzyme Activation
  • Humans
  • Immunity, Innate
  • Inflammation / immunology*
  • Inflammation / metabolism
  • Keratinocytes / immunology
  • Keratinocytes / metabolism
  • Mice
  • Multiprotein Complexes / metabolism
  • Nod Signaling Adaptor Proteins / metabolism*
  • Skin / cytology
  • Skin / immunology
  • Skin / radiation effects*
  • Ultraviolet Rays / adverse effects*


  • Multiprotein Complexes
  • Nod Signaling Adaptor Proteins
  • Caspase 1