| First Author | Schonthaler HB | Year | 2013 |
| Journal | Immunity | Volume | 39 |
| Issue | 6 | Pages | 1171-81 |
| PubMed ID | 24332034 | Mgi Jnum | J:209293 |
| Mgi Id | MGI:5566931 | Doi | 10.1016/j.immuni.2013.11.011 |
| Citation | Schonthaler HB, et al. (2013) S100A8-S100A9 protein complex mediates psoriasis by regulating the expression of complement factor C3. Immunity 39(6):1171-81 |
| abstractText | 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. |
