Journal
JOURNAL OF IMMUNOLOGY
Volume 186, Issue 6, Pages 3304-3308Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.1004122
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Funding
- Swiss National Science Foundation
- Medical Research Council-UK
- Croatian Ministry of Science, Education and Sports
- INSERM, Centre National de la Recherche Scientifique
- Universite de la Mediterranee
- MRC [G0200284, G0802068] Funding Source: UKRI
- Medical Research Council [G0802068, G1000758, G1000758B, G0600698B, G0200284] Funding Source: researchfish
- National Institute for Health Research [NF-SI-0508-10212] Funding Source: researchfish
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It is uncertain whether NK cells modulate T cell memory differentiation. By using a genetic model that allows the selective depletion of NK cells, we show in this study that NK cells shape CD8(+) T cell fate by killing recently activated CD8(+)T cells in an NKG2D- and perforin-dependent manner. In the absence of NK cells, the differentiation of CD8(+) T cells is strongly biased toward a central memory T cell phenotype. Although, on a per-cell basis, memory CD8(+) T cells generated in the presence or the absence of NK cells have similar functional features and recall capabilities, NK cell deletion resulted in a significantly higher number of memory Ag-specific CD8(+) T cells, leading to more effective control of tumors carrying model Ags. The enhanced memory responses induced by the transient deletion of NK cells may provide a rational basis for the design of new vaccination strategies. The Journal of Immunology, 2011, 186: 3304-3308.
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