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.