January 1995 | Mark R. Alderson, Teresa W. Tough, Terri Davis-Smith, Steve Braddy, Ben Falk, Kenneth A. Schooley, Raymond G. Goodwin, Craig A. Smith, Fred Ramsdell, and David H. Lynch
The study investigates the role of Fas ligand (Fas-L) in activation-induced cell death (AICD) in human T lymphocytes. The authors demonstrate that Fas-L expression is induced in previously activated T cells upon stimulation with the CD3/T cell receptor complex, leading to cytolysis. They show that Fas-L antagonists can block AICD in T cell clones and staphylococcal enterotoxin B (SEB)-specific T cell lines. The findings suggest that Fas/Fas-L interactions mediate AICD in activated T cells, providing insights into the mechanisms of peripheral T cell deletion and maintenance of self-tolerance. The study also highlights the potential therapeutic implications of targeting Fas/Fas-L interactions in autoimmune diseases and HIV infection.The study investigates the role of Fas ligand (Fas-L) in activation-induced cell death (AICD) in human T lymphocytes. The authors demonstrate that Fas-L expression is induced in previously activated T cells upon stimulation with the CD3/T cell receptor complex, leading to cytolysis. They show that Fas-L antagonists can block AICD in T cell clones and staphylococcal enterotoxin B (SEB)-specific T cell lines. The findings suggest that Fas/Fas-L interactions mediate AICD in activated T cells, providing insights into the mechanisms of peripheral T cell deletion and maintenance of self-tolerance. The study also highlights the potential therapeutic implications of targeting Fas/Fas-L interactions in autoimmune diseases and HIV infection.