Transcriptional insights into the CD8+ T cell response to infection and memory T cell formation

被引:253
作者
Best, J. Adam [1 ]
Blair, David A. [2 ]
Knell, Jamie [1 ]
Yang, Edward [1 ]
Mayya, Viveka [2 ]
Doedens, Andrew [1 ]
Dustin, Michael L. [2 ]
Goldrath, Ananda W. [1 ]
机构
[1] Univ Calif San Diego, Div Biol Sci, La Jolla, CA 92093 USA
[2] NYU, Sch Med, Skirball Inst Biomol Med, New York, NY USA
基金
美国国家卫生研究院;
关键词
SELECTIVE EXPRESSION; GENE-EXPRESSION; CUTTING EDGE; E-CADHERIN; EFFECTOR; ANTIGEN; DIFFERENTIATION; PRECURSOR; RECEPTOR; IDENTIFICATION;
D O I
10.1038/ni.2536
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
After infection, many factors coordinate the population expansion and differentiation of CD8(+) effector and memory T cells. Using data of unparalleled breadth from the Immunological Genome Project, we analyzed the CD8(+) T cell transcriptome throughout infection to establish gene-expression signatures and identify putative transcriptional regulators. Notably, we found that the expression of key gene signatures can be used to predict the memory-precursor potential of CD8(+) effector cells. Long-lived memory CD8(+) cells ultimately expressed a small subset of genes shared by natural killer T and TB T cells. Although distinct inflammatory milieu and T cell precursor frequencies influenced the differentiation of CD8(+) effector and memory populations, core transcriptional signatures were regulated similarly, whether polyclonal or transgenic, and whether responding to bacterial or viral model pathogens. Our results provide insights into the transcriptional regulation that influence memory formation and CD8(+) T cell immunity.
引用
收藏
页码:404 / 412
页数:9
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