Abstract
Abstract Memory CD4+ T cells specific for a particular antigen can survive for a lifetime of an individual through undefined mechanisms. Previously we have demonstrated that memory CD4+ T cells undergo a state of dormancy during the resolution of infection, and dormant memory T cells survive for the life of mice. To gain an understanding of the genetic programs involved, we examined gene expression profile of memory DO11.10 CD4+ T cells in mice infected with Vaccinia-OVA virus 10.5 months post infection and compared it with gene expression in age-matched old mice. Extensive literature search allowed reverse engineering of genetic network of differentially expressed genes in long-term memory T cells. Pattern of gene expression pointed to the induction of anti-apoptotic and genomic stability pathways. We found that in long term memory CD4+ T cells a shift from glucose to lipid metabolism occurs, along with upregulation of ceramide synthesis and utilization that may favor memory T cell survival. Insulin resistance appears to play a major role in downregulation of glucose metabolism. In conclusion, our data show that in long-term memory CD4+ T cells several major regulatory genes that regulate anti-apoptotic, genomic stability, glucose and lipid metabolism pathways are upregulated and possibly coordinate an overall pro-survival effect.
Published Version
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