期刊
JOURNAL OF IMMUNOLOGY
卷 188, 期 8, 页码 3829-3838出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.1103329
关键词
-
类别
资金
- National Cancer Institute [CA115882]
- Cancer Research Institute, University of Virginia Cancer Center [P30 CA44579]
- Cancer Research UK [C328/A2738, C328/A2737]
- National Institute for Health Research [RP-PG-0310-1003] Funding Source: researchfish
- Grants-in-Aid for Scientific Research [22240089] Funding Source: KAKEN
Fully functional CD8(+) T cell memory is highly dependent upon CD4(+) T cell support. CD4(+) T cells play a critical role in inducing the expression of CD70, the ligand for CD27, on dendritic cells. In this study, we demonstrate that CD27 stimulation during primary CD8(+) T cell responses regulates the ability to mount secondary CD8(+) T cell responses. CD27 stimulation during vaccinia and dendritic cell immunization controls the expression of the IL-7R (CD127), which has been shown to be necessary for memory CD8(+) T cell survival. Furthermore, CD27 stimulation during primary CD8(+) T cell responses to vaccinia virus restrained the late expression on memory precursor cells of cytokine receptors that support terminal differentiation. The formation of CD8(+) T cell memory precursors and secondary CD8(+) T cell responses was restored in the absence of CD27 costimulation when endogenous IL-12 was not available. Similarly, the lesion in CD8(+) T cell memory that occurs in the absence of CD4(+) T cells did not occur in mice lacking IL-12. These data indicate that CD4(+) T cell help and, by extension, CD27 stimulation support CD8(+) T cell memory by modulating the expression of cytokine receptors that influence the differentiation and survival of memory CD8(+) T cells. The Journal of Immunology, 2012, 188: 3829-3838.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据