Sunburned skin activates inflammasomes.
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.
Faustin
Benjamin
B
Burnham Institute for Medical Research, La Jolla, CA 92037, USA.
Reed
John C
JC
D000818:Animals; D020170:Caspase 1 / Q000378:metabolism*; D004789:Enzyme Activation; D006801:Humans; D007113:Immunity, Innate; D007249:Inflammation / Q000276:immunology* / Q000378:metabolism; D015603:Keratinocytes / Q000276:immunology / Q000378:metabolism; D051379:Mice; D046912:Multiprotein Complexes / Q000378:metabolism; D053472:Nod Signaling Adaptor Proteins / Q000378:metabolism*; D012867:Skin / Q000166:cytology / Q000276:immunology / Q000528:radiation effects*; D014466:Ultraviolet Rays / Q000009:adverse effects*
D046912:Multiprotein Complexes; D053472:Nod Signaling Adaptor Proteins; D020170:Caspase 1