Journal
JOURNAL OF EXPERIMENTAL MEDICINE
Volume 198, Issue 12, Pages 1797-1806Publisher
ROCKEFELLER UNIV PRESS
DOI: 10.1084/jem.20030735
Keywords
CD4 memory; cell subsets; T cell survival; homeostasis
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Funding
- NIAID NIH HHS [AI32978, AI41079, P01 AI046530, AI45809, AI46530, R01 AI045809] Funding Source: Medline
- NIA NIH HHS [AG20186, R01 AG020186] Funding Source: Medline
- NIDDK NIH HHS [R01 DK059438, DK59438] Funding Source: Medline
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Cytokines, particularly those of the common gamma chain receptor family, provide extrinsic signals that regulate naive CD4 cell survival. Whether these cytokines are required for the maintenance of memory CD4 cells has not been rigorously assessed. In this paper, we examined the contribution of interleukin (IL) 7, a constitutively produced common gamma chain receptor cytokine, to the survival of resting T cell receptor transgenic memory CD4 cells that were generated in vivo. IL-7 mediated the survival and up-regulation of Bcl-2 by resting memory CD4 cells in vitro in the absence of proliferation. Memory CD4 cells persisted for extended periods upon adoptive transfer into intact or lymphopenic recipients, but not in IL-7(-) mice or in recipients that were rendered deficient in IL-7 by antibody blocking. Both central (CD62L(+)) and effector (CD62L(-)) memory phenotype CD4 cells required IL-7 for survival and, in vivo, memory cells were comparable to naive CD4 cells in this regard. Although the generation of primary effector cells from naive CD4 cells and their dissemination to nonlymphoid tissues were not affected by IL-7 deficiency, memory cells failed to subsequently develop in either the lymphoid or nonlymphoid compartments. The results demonstrate that IL-7 can have previously unrecognized roles in the maintenance of memory in the CD4 cell population and in the survival of CD4 cells with a capacity to become memory cells.
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