| First Author | Li Q | Year | 2010 |
| Journal | J Am Soc Nephrol | Volume | 21 |
| Issue | 8 | Pages | 1344-53 |
| PubMed ID | 20651167 | Mgi Jnum | J:185916 |
| Mgi Id | MGI:5430491 | Doi | 10.1681/ASN.2009090977 |
| Citation | Li Q, et al. (2010) Deficiency of C5aR prolongs renal allograft survival. J Am Soc Nephrol 21(8):1344-53 |
| abstractText | Interaction between C5a, a product of complement activation, and its receptor (C5aR) upregulates antigen-specific T cell responses by modulating the activation of antigen-presenting cells and T cells. Whether this C5a-C5aR interaction contributes to the immune responses that promote renal allograft rejection is unknown. Here, we found that deficiency of C5aR in both graft and recipient reduced allospecific T cell responses and prolonged renal allograft survival. In addition, lack of C5aR impaired the function of donor and recipient antigen-presenting cells and inhibited the response of recipient T cells to allostimulation. Furthermore, deficiency of C5aR in both graft and recipient reduced early inflammation in the grafts, with less cellular infiltration around the vessels and fewer F4/80 positive cells in the peritubular interstitium. These data demonstrate that C5aR is critical for a full adaptive immune response and mediates renal allograft rejection. Engagement of C5aR on dendritic cells and T cells modulates their function, enhancing allospecific T cell responses that lead to allograft rejection. Targeting C5a signaling may have therapeutic potential for T cell-mediated graft rejection. |
