| First Author | Buentke E | Year | 2006 |
| Journal | Blood | Volume | 108 |
| Issue | 6 | Pages | 1949-56 |
| PubMed ID | 16705084 | Mgi Jnum | J:138067 |
| Mgi Id | MGI:3804134 | Doi | 10.1182/blood-2006-04-016857 |
| Citation | Buentke E, et al. (2006) Do CD8 effector cells need IL-7R expression to become resting memory cells?. Blood 108(6):1949-56 |
| abstractText | The role for IL-7R expression in the differentiation of effector T cells into resting memory remains controversial. Here, using a conditional IL-7R transgenic model, we were able to test directly whether CD8 effector T cells require IL-7R expression for their differentiation into resting memory cells. In the absence of IL-7R expression, effector cells transferred into 'full' hosts underwent a protracted and unremitting contraction compared with IL-7R-expressing control cells and were unable to develop into long-term resting memory cells. Surprisingly, when the same effector cells were transferred into empty T-cell-deficient hosts, they could generate long-lived fully functional resting memory cells independently of IL-7R expression. Formation of these latter cells was found to be dependent on IL-15, because the same IL-7R-deficient effector cells were rapidly lost from IL-15-deficient hosts, having a half-life of less than 40 hours. Therefore, our data suggest that, under physiological conditions, both IL-7 and IL-15 synergize to promote the formation of memory cells directly by limiting the contraction of effectors that occurs following an immune response and that reexpression of IL-7R is a key checkpoint in the regulation of this process. |
