Bn. Dittel et al., Evidence for Fas-dependent and Fas-independent mechanisms in the pathogenesis of experimental autoimmune encephalomyelitis, J IMMUNOL, 162(11), 1999, pp. 6392-6400
To determine whether Fas or Fas ligand (FasL) plays a role in susceptibilit
y to experimental autoimmune encephalomyelitis (EAE), we bred a TCR transge
nic mouse specific for the Acl-11 peptide of myelin basic protein to mice w
ith inactivating mutations in Fas (lpr) or Fast (gld), Disease induction by
peptide immunization in such mice produced similar disease scores, demonst
rating that Fas/FasL interactions were not necessary to generate EAE, Howev
er, adoptive transfer experiments showed evidence that these interactions c
an play a role in the pathogenesis of EAE, shown most dramatically by the a
bsence of disease following transfer of cells from a normal myelin basic pr
otein TCR transgenic mouse into a Fas-deficient lpr recipient. Furthermore,
transfer of cells lacking Fast (gld) into normal or gld recipients gave a
diminished disease score. Thus, Fas/FasL interactions can play a role in th
e pathogenesis of EAE, but they are not required for disease to occur.