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CUTTING EDGE |
1
Section of Immunobiology, Yale University School of Medicine, New Haven, CT 06520
As memory CD8 T cells form during acute viral infection, several changes in gene expression and function occur, but little is known about the control of this process. It was reported previously that the homodimer CD8
was involved in generating IL-7Rhigh memory CD8 T cell precursors, and consequently, protective memory CD8 T cells did not form in animals significantly impaired in CD8 expression (E8I–/– mice). However, the precise contribution of CD8 to sustained IL-7R expression and other memory CD8 T cell-associated changes has not been investigated. We found that IL-7R expression and generation of memory CD8 T cells that protect against secondary viral infection was considerably normal in E8I–/– animals. Interestingly, virus-specific CD4 T cell responses were elevated, and the relative surface levels of CD8
in activated T cells were reduced in E8I–/– mice compared with wild-type animals. Our results indicate that memory CD8 T cell development can occur independently of CD8.
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