期刊
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
卷 109, 期 30, 页码 12123-12128出版社
NATL ACAD SCIENCES
DOI: 10.1073/pnas.1201453109
关键词
common gamma c-cytokine; T-cell receptor signaling; CD8 effector differentiation; transcription factors; Jak3
资金
- Center for Cancer Research, National Cancer Institute/National Institutes of Health
- Grants-in-Aid for Scientific Research [24591662] Funding Source: KAKEN
We recently demonstrated that differentiation of cytotoxic T cells requires cooperation between T-cell receptor (TCR)/costimulation and gamma c-cytokines. Here we demonstrate that the transcription factor IFN regulatory factor 8 (IRF8) is expressed in CD8 T cells by the combination of these two signals. More importantly, depletion of IRF8 in these cells abrogated the differentiation of naive CD8 T cells into effector cells in an experimental graft-vs.-host disease mouse model. We also show that IRF8 seems to not operate upstream of other critical factors such as T-bet and eomesodermin, which have been implicated in effector maturation. Collectively, our work shows that IRF8 integrates the TCR/costimulation and gamma c-cytokine- signaling pathways and mediates the transition of naive CD8 T cells to effector cells, thus identifying IRF8 as one of the molecular regulators of CD8 T-cell differentiation.
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