Massive upregulation of the Fas ligand in lpr and gld mice: implications for Fas regulation and the graft-versus-host disease-like wasting syndrome

@article{Chu1995MassiveUO,
  title={Massive upregulation of the Fas ligand in lpr and gld mice: implications for Fas regulation and the graft-versus-host disease-like wasting syndrome},
  author={Jia Li Chu and Paloma Ramos and Adam Rosendorff and Janko Nikoli{\'c}-Z̆ugi{\'c} and Elizabeth H Lacy and Akio Matsuzawa and Keith B Elkon},
  journal={The Journal of Experimental Medicine},
  year={1995},
  volume={181},
  pages={393 - 398}
}
Fas-deficient lpr and gld mice develop lymphadenopathy due to the accumulation of T cells with an unusual double negative (DN) (CD4-CD8-) phenotype. Previous studies have shown that these abnormal cells are capable of inducing redirected lysis of certain Fc receptor-positive target cells. Since the Fas ligand (FasL) has recently been shown to be partly responsible for T cell-mediated cytotoxicity, lymph node cells from lpr and gld mice were examined for the expression of FasL mRNA. Northern… CONTINUE READING

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