Resolution of infection promotes a state of dormancy and long survival of CD4 memory T cells

Sarat K. Dalai, Stanislav Khoruzhenko, Charles G. Drake, Chunfa C. Jie, Scheherazade Sadegh-Nasseri

Research output: Contribution to journalArticlepeer-review


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 languageEnglish (US)
Pages (from-to)870-881
Number of pages12
JournalImmunology and Cell Biology
Issue number8
StatePublished - Nov 2011


  • 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


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