| First Author | Lamy L | Year | 2007 |
| Journal | J Immunol | Volume | 178 |
| Issue | 9 | Pages | 5930-9 |
| PubMed ID | 17442977 | Mgi Jnum | J:145825 |
| Mgi Id | MGI:3836120 | Doi | 10.4049/jimmunol.178.9.5930 |
| Citation | Lamy L, et al. (2007) Interactions between CD47 and thrombospondin reduce inflammation. J Immunol 178(9):5930-9 |
| abstractText | CD47 on the surface of T cells was shown in vitro to mediate either T cell activation or, in the presence of high amounts of thrombospondin (TSP), T cell apoptosis. We report here that CD47-deficient mice, as well as TSP-1 or TSP-2-deficient mice, sustain oxazolone-induced inflammation for more than four days, whereas wild-type mice reduce the inflammation within 48 h. We observe that prolonged inflammation in CD47-, TSP-1-, or TSP-2-deficient mice is accompanied by a local deficiency of T cell apoptosis. Finally, we show that upon activation normal T cells increase the expression of the proapoptotic Bcl-2 family member BNIP3 (Bcl-2/adenovirus E1B 19-kDa interacting protein) and undergo CD47-mediated apoptosis. This finding is consistent with our previous demonstration of a physical interaction between BNIP3 and CD47 that inhibits BNIP3 degradation by the proteasome, sensitizing T cells to CD47-induced apoptosis. Overall, these results reveal an important role in vivo for this new CD47/BNIP3 pathway in limiting inflammation by controlling the number of activated T cells. |
