| First Author | Wenderfer SE | Year | 2009 |
| Journal | Mol Immunol | Volume | 46 |
| Issue | 7 | Pages | 1397-404 |
| PubMed ID | 19167760 | Mgi Jnum | J:148299 |
| Mgi Id | MGI:3844200 | Doi | 10.1016/j.molimm.2008.12.004 |
| Citation | Wenderfer SE, et al. (2009) C3a receptor deficiency accelerates the onset of renal injury in the MRL/lpr mouse. Mol Immunol 46(7):1397-404 |
| abstractText | The development and progression of systemic lupus erythematosus (SLE) is strongly associated with complement activation and deposition. The anaphylatoxin C3a is a product of complement activation with immunomodulatory properties, and the receptor for C3a (C3aR) is not only expressed by granulocytes and antigen presenting cell populations, but it is also strongly up-regulated in lupus prone mice with active nephritis. In order to characterize the role of the C3aR in inflammatory nephritis, we bred C3aR knock out mice onto the MRL/lpr genetic background (C3aR KO MRL). Compared to control MRL/lpr mice, C3aR KO MRL mice had elevated auto-antibody titers and an earlier onset of renal injury. At 8 weeks, renal expression of a wide range of chemokines and chemokine receptors was increased in C3aR KO MRL kidneys compared to controls. Only the expression of MCP-1 was significantly decreased in the C3aR KO MRL mice. The increased chemokine and chemokine receptor expression seen in the C3aR KO MRL mice was associated with a more rapid rise in serum creatinine and the acceleration of renal fibrosis. However, loss of the C3aR had little impact on long-term kidney injury and did not alter survival. These findings suggest that activation of the C3aR plays a protective, not pathologic, role in the early phase of inflammatory nephritis in the MRL/lpr model of SLE. |
