| First Author | Gerard NP | Year | 2005 |
| Journal | J Biol Chem | Volume | 280 |
| Issue | 48 | Pages | 39677-80 |
| PubMed ID | 16204243 | Mgi Jnum | J:104092 |
| Mgi Id | MGI:3611130 | Doi | 10.1074/jbc.C500287200 |
| Citation | Gerard NP, et al. (2005) An anti-inflammatory function for the complement anaphylatoxin C5a-binding protein, C5L2. J Biol Chem 280(48):39677-80 |
| abstractText | C5L2 is an enigmatic serpentine receptor that is co-expressed with the C5a receptor on many cells including polymorphonuclear neutrophils. The apparent absence of coupling of C5L2 with G proteins suggests that this receptor may modulate the biological activity of C5a, perhaps by acting as a decoy receptor. Alternatively, C5L2 may affect C5a function through formation of a heteromeric complex with the C5aR, or it may utilize a G protein-independent signaling pathway. Here we show that in mice bearing a targeted deletion of C5L2, the biological activity of C5a/C5a(desArg) is enhanced both in vivo and in vitro. The biological role of C5L2 thus appears to be limiting to the pro-inflammatory response to the anaphylatoxin. Accordingly, up-regulation of C5L2 may be of benefit in inflammatory states driven by C5a, including sepsis, asthma, cystic fibrosis, and chronic obstructive lung disease. |
