| First Author | Xu R | Year | 2010 |
| Journal | Eur J Immunol | Volume | 40 |
| Issue | 4 | Pages | 1079-88 |
| PubMed ID | 20140904 | Mgi Jnum | J:159188 |
| Mgi Id | MGI:4441561 | Doi | 10.1002/eji.200940015 |
| Citation | Xu R, et al. (2010) Complement C5a regulates IL-17 by affecting the crosstalk between DC and gammadelta T cells in CLP-induced sepsis. Eur J Immunol 40(4):1079-88 |
| abstractText | Complement 5a (C5a) and Interleukin-17 (IL-17) are two important inflammatory mediators in sepsis. Here we studied the mechanisms underlying regulation of IL-17 by anaphylatoxin C5a. We found that C5a blockade increased the survival rate of mice following cecal ligation and puncture (CLP)-induced sepsis and decreased IL-17 expression in vivo. IL-17 was secreted mainly by gammadelta T cells in this model. Importantly, our data suggest that C5a participates in the regulation of IL-17 secretion by gammadelta T cells. Dendritic cells (DC) were found to act as a 'bridge' between C5a and gammadelta T cells in a mechanism involving IL-6 and transforming growth factor beta (TGF-beta). These results imply that C5a affects the crosstalk between DC and gammadelta T cells during sepsis development, and this may result in a large production of inflammatory mediators such as IL-17. |
