Journal
JOURNAL OF IMMUNOLOGY
Volume 188, Issue 8, Pages 3639-3647Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.1101580
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Funding
- American Cancer Society [ACSLIB112496-RSG]
- American Cancer Society-Illinois Division [07-20]
- National Institutes of Health [R21CA127037-01A1, 1P01CA154778-01A1, AI007090]
- Cancer Research Foundation
- National Cancer Institute [5P30CA014599-35]
- University of Chicago
- Loyola University Chicago
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CD8(+) T cell responses have been shown to be regulated by dendritic cells (DCs) and CD4(+) T cells, leading to the tenet that CD8(+) T cells play a passive role in their own differentiation. In contrast, by using a DNA vaccination model, to separate the events of vaccination from those of CD8(+) T cell priming, we demonstrate that CD8(+) T cells, themselves, actively limit their own memory potential through CD8(+) T cell-derived IFN-gamma-dependent modification of the IL-12/IL-15R alpha axis on DCs. Such CD8(+) T cell-driven cytokine alterations result in increased T-bet and decreased Bcl-2 expression, and thus decreased memory progenitor formation. These results identify an unrecognized role for CD8(+) T cells in the regulation of their own effector differentiation fate and a previously uncharacterized relationship between the balance of inflammation and memory formation. The Journal of Immunology, 2012, 188: 3639-3647.
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