Abstract
Activated murine cytotoxic T cells express the NKG2D natural cytotoxicity receptor. This receptor recognizes major histocompatibility complex (MHC) class I–like molecules expressed on the surface of infected cells and serves to augment T cell–mediated cytotoxicity. The role of NKG2D-mediated augmentation in the clearance of central nervous system viral infections has not been explored. Using the Theiler's murine encephalomyelitis virus model, the authors found that NKG2D-positive CD8+ cytotoxic T cells enter the brain, that NKG2D ligands are expressed in the brain during acute infection, and that interruption of NKG2D ligand recognition via treatment with a function-blocking antibody attenuates the efficacy of viral clearance from the central nervous system.
The authors are grateful to Reghann LaFrance-Corey for expert technical assistance and to Nikilyn Kinzel for conceptual, textual, and experimental guidance. This work was supported by a grant from the National Multiple Sclerosis Society (RG3636), by an early career development award from the Mayo Clinic (CLH), and by Donald and Frances Herdrich.