| First Author | Diaz-Guerra E | Year | 2007 |
| Journal | J Immunol | Volume | 179 |
| Issue | 11 | Pages | 7352-7 |
| PubMed ID | 18025178 | Mgi Jnum | J:154819 |
| Mgi Id | MGI:4399007 | Doi | 10.4049/jimmunol.179.11.7352 |
| Citation | Diaz-Guerra E, et al. (2007) CCL2 inhibits the apoptosis program induced by growth factor deprivation, rescuing functional T cells. J Immunol 179(11):7352-7 |
| abstractText | The precise mechanisms involved in the switch between the clonal expansion and contraction phases of a CD8(+) T cell response remain to be fully elucidated. One of the mechanisms implicated in the contraction phase is cytokine deprivation, which triggers apoptosis in these cells. CCR2 chemokine receptor is up-regulated following IL-2 deprivation, and its ligand CCL2 plays an essential role preventing apoptosis induced by IL-2 withdrawal not only in CTLL2 cells, but also in mouse Ag-activated primary CD8(+) T cells because it rescued functional CD8(+) T cells from deprivation induced apoptosis, promoting proliferation in response to subsequent addition of IL-2 or to secondary antigenic challenges. Thus, up-regulation of the CCR2 upon growth factor withdrawal together with the protective effects of CCL2, represent a double-edged survival strategy, protecting cells from apoptosis and enabling them to migrate toward sites where Ag and/or growth factors are available. |
