CD8αα homodimer expression and role in CD8 T cell memory generation during influenza virus A infection in mice

While the precise function of CD8 alpha alpha homodimer expression on peripheral T cells is uncertain, recent evidence indicates that it facilitates survival and differentiation of lymphocytic choriomeningitis virus (LCMV)-specific memory CD8 alpha beta T cell precursors in vivo. Here, we show that the CD8 alpha alpha homodimer is also transiently up-regulated on influenza A virus-specific CD8 alpha beta T cells after infection in vivo, temporally correlating with increased levels of the memory T cell development- and survival-related molecules IL-7R alpha and Bcl-2, respectively. Unlike with LCMV, however, deletion of the CD8 alpha alpha enhancer I does not abrogate CD8 alpha alpha homodimer expression or manifest a significant impact on the generation of virus-specific, functional effector and central memory T cells in influenza A virus infection. These results demonstrate that the role of CD8 alpha alpha in the generation of antiviral CD8 T cell memory is complex, presumably because various viral stimuli differentially regulate CD8 alpha alpha expression. Further studies are needed to define those ligands that induce CD8 alpha alpha on T cells during acute viral infections, and the general relevance of this process to memory T cell formation.