期刊
IMMUNOLOGY AND CELL BIOLOGY
卷 89, 期 8, 页码 870-881出版社
WILEY
DOI: 10.1038/icb.2011.2
关键词
BCR-mediated antigen capture; CD4 memory T cells; gene regulation; low-dose antigen; memory survival
资金
- [R01GM53549]
- [R01AI063764]
Memory T cells survive throughout the lifetime of an individual and are protective upon recall. It is not clear how memory T cells can live so long. Here, we demonstrate that at the resolution of a viral infection, low levels of antigen are captured by B cells and presented to specific CD4(+) memory T cells to render a state of unresponsiveness. We demonstrate in two systems that this process occurs naturally during the fall of antigen and is associated with a global gene expression program initiated with the clearance of antigen. Our study suggests that in the absence of antigen, a state of dormancy associated with low-energy utilization and proliferation can help memory CD4(+) T cells to survive nearly throughout the lifetime of mice. The dormant CD4(+) memory T cells become activated by stimulatory signals generated by a subsequent infection. We propose that quiescence might be a mechanism necessary to regulate long-term survival of CD4 memory T cells and to prevent cross-reactivity to self, hence autoimmunity. Immunology and Cell Biology (2011) 89, 870-881; doi:10.1038/icb.2011.2; published online 1 March 2011
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