Generation of cellular immunity to lymphocytic choriomeningitis virus is independent of CD1d1 expression

CD1 molecules are cell surface glycoproteins, structurally similar to major histocompatibility complex (MHC) class I molecules. The murine CD1d1 molec ule has been shown to be essential for the positive selection of a unique s ubpopulation of T cells [the natural killer (NK) T cells], as CD1d1-deficie nt mice lack NK T cells. These cells have recently been suggested to play a n important role in the induction of innate immunity (i.e. NK cells) and th e regulation of immune homeostasis. As such, it was asked whether NK T cell s were necessary for the generation of cellular immunity to an acute virus infection. In these studies, the Armstrong strain of lymphocytic choriomeni ngitis virus (LCMV), a classic inducer of NK cells, and its pathogenic vari ant clone 13 were used. When NK-cell activity was assessed on day 3 post-LC MV infection, surprisingly, it was found that CD1d1-deficient mice could ge nerate NK-cell activity at wild-type levels. Likewise, LCMV-specific cytoto xic T-lymphocyte (CTL) activity in CD1d1-deficient mice was indistinguishab le from that generated in wild-type mice. Additionally, viral titres in the spleen (LCMV Armstrong) and blood (LCMV clone 13) of infected CD1d1-defici ent mice were at comparable levels to those found in wild-type mice, as wer e virus infection-induced increases in cell surface H-2K(b) in the spleen. Therefore, these results suggest that the LCMV-induced generation of NK-cel l and virus-specific CTL activity, as well as viral clearance, are independ ent of CD1d1 expression.