Effector and memory CD8+ T cell fate coupled by T-bet and eomesodermin
Copyright policy )Effector and memory CD8+ T cell fate coupled by T-bet and eomesodermin
Two seemingly unrelated hallmarks of memory CD8(+) T cells are cytokine-driven proliferative renewal after pathogen clearance and a latent effector program in anticipation of rechallenge. Memory CD8(+) T cells and natural killer cells share cytotoxic potential and dependence on the growth factor interleukin 15. We now show that mice with compound mutations of the genes encoding the transcription factors T-bet and eomesodermin were nearly devoid of several lineages dependent on interleukin 15, including memory CD8(+) T cells and mature natural killer cells, and that their cells had defective cytotoxic effector programming. Moreover, T-bet and eomesodermin were responsible for inducing enhanced expression of CD122, the receptor specifying interleukin 15 responsiveness. Therefore, these key transcription factors link the long-term renewal of memory CD8(+) T cells to their characteristic effector potency.
- University of California, San Diego United States
- Yale University United States
- University of Oxford United Kingdom
- University of Pennsylvania United States
- University of Colorado Cancer Center United States
Interleukin-15, Mice, Knockout, Mice, Transgenic, Receptors, Interleukin-2, CD8-Positive T-Lymphocytes, Mice, Inbred C57BL, Mice, Phenotype, Animals, Humans, T-bet Transcription Factor, T-Box Domain Proteins, Immunologic Memory, Cells, Cultured, Transcription Factors
Interleukin-15, Mice, Knockout, Mice, Transgenic, Receptors, Interleukin-2, CD8-Positive T-Lymphocytes, Mice, Inbred C57BL, Mice, Phenotype, Animals, Humans, T-bet Transcription Factor, T-Box Domain Proteins, Immunologic Memory, Cells, Cultured, Transcription Factors
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