Enhanced antiviral T cell function in the absence of B7-H1 is insufficient to prevent persistence but exacerbates axonal bystander damage during viral encephalomyelitis.

@article{Phares2010EnhancedAT,
  title={Enhanced antiviral T cell function in the absence of B7-H1 is insufficient to prevent persistence but exacerbates axonal bystander damage during viral encephalomyelitis.},
  author={Timothy W. Phares and Stephen A. Stohlman and David R Hinton and Roscoe A. Atkinson and Cornelia C. Bergmann},
  journal={Journal of immunology},
  year={2010},
  volume={185 9},
  pages={5607-18}
}
The T cell inhibitory ligand B7-H1 hinders T cell-mediated virus control, but also ameliorates clinical disease during autoimmune and virus-induced CNS disease. In mice infected with gliatropic demyelinating coronavirus, B7-H1 expression on oligodendroglia delays virus control, but also dampens clinical disease. To define the mechanisms by which B7-H1 alters pathogenic outcome, virus-infected B7-H1-deficient (B7-H1(-/-)) mice were analyzed for altered peripheral and CNS immune responses. B7-H1… CONTINUE READING
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