The use of double IFN-γ-YFP+ and IL-10-GFP+ reporter mice have indicated that following resolution of primary infection, the stability and potential of CD4+ IFNγ+ IL-10+ T cells to become memory is limited [320], in part because they exhibit an exhaustion phenotype and are generally unresponsive at the early stage of secondary infection. This evidence concerns the gene CD4 and infection.