| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 2204936 | Trends in Cell Biology | 2008 | 5 Pages |
Abstract
Ultraviolet (UV) irradiation injures the epidermis, resulting in sunburn and inflammation. UV-irradiated keratinocytes secrete interleukin-1β 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.
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Authors
Benjamin Faustin, John C. Reed,