| First Author | Dunkelberger J | Year | 2012 |
| Journal | J Immunol | Volume | 188 |
| Issue | 8 | Pages | 4032-42 |
| PubMed ID | 22430734 | Mgi Jnum | J:184056 |
| Mgi Id | MGI:5320210 | Doi | 10.4049/jimmunol.1103141 |
| Citation | Dunkelberger J, et al. (2012) C5aR expression in a novel GFP reporter gene knockin mouse: implications for the mechanism of action of C5aR signaling in T cell immunity. J Immunol 188(8):4032-42 |
| abstractText | C5aR is a G protein-coupled receptor for the anaphylatoxin C5a and mediates many proinflammatory reactions. C5aR signaling also has been shown to regulate T cell immunity, but its sites and mechanism of action in this process remain uncertain. In this study, we created a GFP knockin mouse and used GFP as a surrogate marker to examine C5aR expression. GFP was knocked into the 3'-untranslated region of C5ar1 by gene targeting. We show that GFP is expressed highly on Gr-1(+)CD11b(+) cells in the blood, spleen, and bone marrow and moderately on CD11b(+)F4/80(+) circulating leukocytes and elicited peritoneal macrophages. No GFP is detected on resting or activated T lymphocytes or on splenic myeloid or plasmacytoid dendritic cells. In contrast, 5-25% cultured bone marrow-derived dendritic cells expressed GFP. Interestingly, GFP knockin prevented cell surface but not intracellular C5aR expression. We conclude that C5aR is unlikely to play an intrinsic role on murine T cells and primary dendritic cells. Instead, its effect on T cell immunity in vivo may involve CD11b(+)F4/80(+) or other C5aR-expressing leukocytes. Further, our data reveal a surprising role for the 3'-untranslated region of C5aR mRNA in regulating C5aR protein targeting to the plasma membrane. |
