| First Author | Badovinac VP | Year | 2006 |
| Journal | J Immunol | Volume | 177 |
| Issue | 2 | Pages | 999-1006 |
| PubMed ID | 16818756 | Mgi Jnum | J:134947 |
| Mgi Id | MGI:3790140 | Doi | 10.4049/jimmunol.177.2.999 |
| Citation | Badovinac VP, et al. (2006) TRAIL deficiency delays, but does not prevent, erosion in the quality of 'helpless' memory CD8 T cells. J Immunol 177(2):999-1006 |
| abstractText | In this study, we investigated the role of TRAIL in Ag-specific CD8 T cell homeostasis after viral infection. TRAIL deficiency does not influence the kinetics of the Ag-specific CD8 T cell responses, and CD8 T cells in TRAIL-deficient mice were able to expand, contract, and generate functional memory cell numbers that were indistinguishable from TRAIL-sufficient wild-type CD8 T cells after acute lymphocytic choriomeningitis virus infection. Interestingly, the ability of 'helpless' CD8 T cells to retain their memory phenotypic and functional (i.e., secondary expansion) characteristics was prolonged in TRAIL-deficient mice compared with wild-type CD4-depleted controls. However, TRAIL deficiency only delayed, but did not prevent, the eventual erosion in the quality of helpless memory CD8 T cells, and that correlated with their inability to respond to a second round of Ag-driven proliferation. These data, which suggest that CD4 help consists of both TRAIL-dependent and -independent components, may help to resolve the current controversy between the early programming and maintenance models that were put forward to explain the role of CD4 T cell help in Ag-specific CD8 T cell homeostasis. |
