Fas ligand mediates activation-induced cell death in human T lymphocytes.
Fas ligand mediates activation-induced cell death in human T lymphocytes.
Alderson, M R; Tough, T W; Davis-Smith, T; Braddy, S; Falk, B; Schooley, K A; Goodwin, R G; Smith, C A; Ramsdell, F; Lynch, D H
1995-01-01 00:00:00
A significant proportion of previously activated human T cells undergo apoptosis when triggered through the CD3/T cell receptor complex, a process termed activation-induced cell death (AICD). Ligation of Fas on activated T cells by either Fas antibodies or recombinant human Fas-ligand (Fas-L) also results in cytolysis. We demonstrate that these two pathways of apoptosis are causally related. Stimulation of previously activated T cells resulted in the expression of Fas-L mRNA and lysis of Fas-positive target cells. Fas-L antagonists inhibited AICD of T cell clones and staphylococcus enterotoxin B (SEB)-specific T cell lines. The data indicate AICD in previously stimulated T cells is mediated by Fas/Fas-L interactions.
http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.pngThe Journal of Experimental MedicineRockefeller University Presshttp://www.deepdyve.com/lp/rockefeller-university-press/fas-ligand-mediates-activation-induced-cell-death-in-human-t-3EFdm2Fjd4
Fas ligand mediates activation-induced cell death in human T lymphocytes.
A significant proportion of previously activated human T cells undergo apoptosis when triggered through the CD3/T cell receptor complex, a process termed activation-induced cell death (AICD). Ligation of Fas on activated T cells by either Fas antibodies or recombinant human Fas-ligand (Fas-L) also results in cytolysis. We demonstrate that these two pathways of apoptosis are causally related. Stimulation of previously activated T cells resulted in the expression of Fas-L mRNA and lysis of Fas-positive target cells. Fas-L antagonists inhibited AICD of T cell clones and staphylococcus enterotoxin B (SEB)-specific T cell lines. The data indicate AICD in previously stimulated T cells is mediated by Fas/Fas-L interactions.
Journal
The Journal of Experimental Medicine
– Rockefeller University Press
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