| First Author | Purton JF | Year | 2007 |
| Journal | J Exp Med | Volume | 204 |
| Issue | 4 | Pages | 951-61 |
| PubMed ID | 17420265 | Mgi Jnum | J:125743 |
| Mgi Id | MGI:3759744 | Doi | 10.1084/jem.20061805 |
| Citation | Purton JF, et al. (2007) Antiviral CD4+ memory T cells are IL-15 dependent. J Exp Med 204(4):951-61 |
| abstractText | Survival and intermittent proliferation of memory CD4(+) and CD8(+) T cells appear to be controlled by different homeostatic mechanisms. In particular, contact with interleukin (IL)-15 has a decisive influence on memory CD8(+) cells, but not memory CD4(+) cells. Past studies of memory CD4(+) cells have relied heavily on the use of naturally occurring memory phenotype (MP) cells as a surrogate for antigen (Ag)-specific memory cells. However, we show here that MP CD4(+) cells contain a prominent subset of rapidly proliferating major histocompatibility complex (MHC) II-dependent cells. In contrast, Ag-specific memory CD4 cells have a slow turnover rate and are MHC II independent. In irradiated hosts, these latter cells ignore IL-15 and expand in response to the elevated levels of IL-7 in the lymphopenic hosts. In contrast, in normal nonlymphopenic hosts where IL-7 levels are low, memory CD4 cells are heavily dependent on IL-15. Significantly, memory CD4(+) responsiveness to endogenous IL-15 reflects marked competition from other cells, especially CD8(+) and natural killer cells, and increases considerably after removal of these cells. Therefore, under normal physiological conditions, homeostasis of CD8(+) and CD4(+) memory cells is quite similar and involves IL-15 and IL-7. |
