期刊
NATURE IMMUNOLOGY
卷 20, 期 12, 页码 1668-+出版社
NATURE PORTFOLIO
DOI: 10.1038/s41590-019-0515-x
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资金
- US National Institutes of Health [RO1 5R01DK074500, P01AI108545, T32 CA207021]
- Howard Hughes Medical Institute Gilliam Fellowship for Advanced Study
Lymph node fibroblastic reticular cells (FRCs) respond to signals from activated T cells by releasing nitric oxide, which inhibits T cell proliferation and restricts the size of the expanding T cell pool. Whether interactions with FRCs also support the function or differentiation of activated CD8(+) T cells is not known. Here we report that encounters with FRCs enhanced cytokine production and remodeled chromatin accessibility in newly activated CD8(+) T cells via interleukin-6. These epigenetic changes facilitated metabolic reprogramming and amplified the activity of pro-survival pathways through differential transcription factor activity. Accordingly, FRC conditioning significantly enhanced the persistence of virus-specific CD8(+) T cells in vivo and augmented their differentiation into tissue-resident memory T cells. Our study demonstrates that FRCs play a role beyond restricting T cell expansion-they can also shape the fate and function of CD8(+) T cells.
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