Fas and Fas ligand enhance the pathogenesis of experimental allergic encephalomyelitis, but are not essential for immune privilege in the central nervous system.

@article{Sabelko1997FasAF,
  title={Fas and Fas ligand enhance the pathogenesis of experimental allergic encephalomyelitis, but are not essential for immune privilege in the central nervous system.},
  author={Kimberly A Sabelko and Kathleen Kelly and Moon H. Nahm and Anne H. Cross and John H. Russell},
  journal={Journal of immunology},
  year={1997},
  volume={159 7},
  pages={3096-9}
}
Mutations of CD95 and CD95L, lpr and gld, respectively, are associated with spontaneous autoimmune disease and alteration of immune privilege. In lpr or gld animals these processes would be expected to exacerbate experimental allergic encephalomyelitis (EAE), an animal model of the autoimmune demyelinating disease multiple sclerosis. However, here we show that the lpr and gld mutations did not overcome the MHC-defined limits of disease and, surprisingly, did not exacerbate the pathology of EAE… CONTINUE READING