Journal
IMMUNITY
Volume 39, Issue 6, Pages 1171-1181Publisher
CELL PRESS
DOI: 10.1016/j.immuni.2013.11.011
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Funding
- Boehringer Ingelheim
- Austrian Science Foundation [NFN S94-SP11]
- Banco Bilbao Vizcaya Argentaria (BBVA) Foundation
- European Research Council Advanced Grant [ERC FCK/2008/37]
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Psoriasis is a common heterogeneous inflammatory skin disease with a complex pathophysiology and limited treatment options. Here we performed proteomic analyses of human psoriatic epidermis and found S100A8-S100A9, also called calprotectin, as the most upregulated proteins, followed by the complement component C3. Both S100A8-S100A9 and C3 are specifically expressed in lesional psoriatic skin. S100A9 is shown here to function as a chromatin component modulating C3 expression in mouse and human cells by binding to a region upstream of the C3 start site. When S100A9 was genetically deleted in mouse models of skin inflammation, the psoriasis-like skin disease and inflammation were strongly attenuated, with a mild immune infiltrate and decreased amounts of C3. In addition, inhibition of C3 in the mouse model strongly reduced the inflammatory skin disease. Thus, S100A8-S100A9 can regulate C3 at the nuclear level and present potential new therapeutic targets for psoriasis.
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