Dittel B N, Merchant R M, Janeway C A
Section of Immunobiology, Yale University School of Medicine, Howard Hughes Medical Institute, New Haven, CT 06520, USA.
J Immunol. 1999 Jun 1;162(11):6392-400.
To determine whether Fas or Fas ligand (FasL) plays a role in susceptibility to experimental autoimmune encephalomyelitis (EAE), we bred a TCR transgenic mouse specific for the Ac1-11 peptide of myelin basic protein to mice with inactivating mutations in Fas (lpr) or FasL (gld). Disease induction by peptide immunization in such mice produced similar disease scores, demonstrating that Fas/FasL interactions were not necessary to generate EAE. However, adoptive transfer experiments showed evidence that these interactions can play a role in the pathogenesis of EAE, shown most dramatically by the absence of disease following transfer of cells from a normal myelin basic protein TCR transgenic mouse into a Fas-deficient lpr recipient. Furthermore, transfer of cells lacking FasL (gld) into normal or gld recipients gave a diminished disease score. Thus, Fas/FasL interactions can play a role in the pathogenesis of EAE, but they are not required for disease to occur.
为了确定Fas或Fas配体（FasL）在实验性自身免疫性脑脊髓炎（EAE）易感性中是否起作用，我们将针对髓鞘碱性蛋白的Ac1-11肽的TCR转基因小鼠与Fas（lpr）或FasL（gld）发生失活突变的小鼠进行杂交。在这些小鼠中通过肽免疫诱导疾病产生了相似的疾病评分，表明Fas/FasL相互作用对于产生EAE并非必需。然而，过继转移实验显示有证据表明这些相互作用可在EAE的发病机制中起作用，最显著的表现是将来自正常髓鞘碱性蛋白TCR转基因小鼠的细胞转移到Fas缺陷的lpr受体中后无疾病发生。此外，将缺乏FasL（gld）的细胞转移到正常或gld受体中会使疾病评分降低。因此，Fas/FasL相互作用可在EAE的发病机制中起作用，但疾病发生并不需要它们。
