| Autor: |
Ramsdell F; Department of Immunobiology, Immunex Research and Development Corporation, Seattle, WA 98101., Seaman MS, Miller RE, Tough TW, Alderson MR, Lynch DH |
| Jazyk: |
angličtina |
| Zdroj: |
European journal of immunology [Eur J Immunol] 1994 Apr; Vol. 24 (4), pp. 928-33. |
| DOI: |
10.1002/eji.1830240422 |
| Abstrakt: |
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. |
| Databáze: |
MEDLINE |
| Externí odkaz: |
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