Abstract
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.
Original language | English (US) |
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Pages (from-to) | 870-881 |
Number of pages | 12 |
Journal | Immunology and Cell Biology |
Volume | 89 |
Issue number | 8 |
DOIs | |
State | Published - Nov 2011 |
Keywords
- BCR-mediated antigen capture
- CD4 memory T cells
- gene regulation
- low-dose antigen
- memory survival
ASJC Scopus subject areas
- Immunology and Allergy
- Immunology
- Cell Biology