| First Author | Ramsdell F | Year | 1994 |
| Journal | Eur J Immunol | Volume | 24 |
| Issue | 4 | Pages | 928-33 |
| PubMed ID | 7512035 | Mgi Jnum | J:17698 |
| Mgi Id | MGI:65729 | Doi | 10.1002/eji.1830240422 |
| Citation | Ramsdell F, et al. (1994) gld/gld mice are unable to express a functional ligand for Fas. Eur J Immunol 24(4):928-33 |
| abstractText | Mice homozygous for either the lpr or gld genes develop phenotypically identical autoimmune disorders. The gene responsible for the pathology in lpr/lpr mice encodes the Fas antigen, a protein associated with the induction of programmed cell death. To determine if the defect associated with gld represents a mutation in the ligand for Fas, we have assessed the ability of lymphoid cells from homozygous gld/gld mice to lyse target cells in a Fas-dependent manner. Using an antagonistic antibody to Fas, we demonstrate that activated T cells from normal and lpr mice are capable of inducing Fas-mediated lysis of tumor target cells. In contrast, activated T cells from gld/gld mice fail to induce lysis of tumor targets, although cells from gld mice are able to lyse specific allogeneic targets following mixed lymphocyte culture. In addition, activated T cells from gld/gld homozygous animals are not capable of binding to a Fas.Fc fusion protein at high levels, whereas activated T cells from normal and lpr/lpr animals bind Fas.Fc efficiently. These data indicate that mice homozygous for gld are unable to express a functional ligand for Fas. |
