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Antiviral CD4+ memory T cells are IL-15 dependent


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.

Type Journal
ISBN 0022-1007 (Print)
Authors Purton, J. F.;Tan, J. T.;Rubinstein, M. P.;Kim, D. M.;Sprent, J.;Surh, C. D. :
Published Date 2007-01-01
Published Volume 204
Published Issue 4
Published Pages 951-61
Status Published in-print
URL link to publisher's version
OpenAccess link to author's accepted manuscript version