期刊
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
卷 99, 期 5, 页码 3001-3006出版社
NATL ACAD SCIENCES
DOI: 10.1073/pnas.052676899
关键词
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资金
- NCI NIH HHS [CA33084, R37 CA033084, R01 CA033084] Funding Source: Medline
- NIAID NIH HHS [AI43650] Funding Source: Medline
Multiple cytokines, including IL-2, can affect T cell proliferation and survival. However, IL-2 can lead to apoptosis as well as proliferation, making unclear whether IL-2 receptor (IL-2R) signals ultimately have a predominantly positive or negative effect. To address this issue, we examined the effect of enhancing IL-2R signals in CD8(+) T cells after antigen stimulation by engineering a transgenic (Tg) mouse strain with CD8(+) T cells capable of augmented, regulated, autocrine IL-2R signaling after target recognition by means of expression of a chimeric granulocyte-macrophage colony-stimulating factor (GM-CSF)/IL-2R. The Tg CD8+ T cells can bind the granulocyte-macrophage colony-stimulating GM-CSF produced by antigen stimulation, but the GM-CSF binding results in delivery of an IL-2R signal. After antigen stimulation in vivo, the Tg T cells demonstrated marked increases in the initial proliferative response and cell expansion and displayed continued increases in cell expansion after repeated antigen exposure. These data suggest that the predominant role of IL-2R signals delivered to responding CD8+ T cells is to set the size of the initial response to antigen by promoting T cell proliferation and survival and not cell death.
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