Fas (CD95)/FasL interactions required for programmed cell death after T-cell activation
ST Ju, DJ Panka, H Cui, R Ettinger, M Ei-Khatib… - Nature, 1995 - nature.com
ST Ju, DJ Panka, H Cui, R Ettinger, M Ei-Khatib, DH Sherr, BZ Stanger, A Marshak-Rothstein
Nature, 1995•nature.comRECEPTOR crosslinking of T-cell hybridomas induces cell activation followed by apoptosis1–
6. This activation-induced cell death requires de novo synthesis of RNA and proteins1–3,
but the actual gene products that provide the death signal have not been identified4–6. We
show here that receptor crosslinking induces Fas ligand and upregulates Fas, and that the
ensuing engagement of Fas by Fas ligand activates the cell-death programme. Cell death,
but not activation, can be selectively prevented by a soluble Fas–immunoglobulin fusion …
6. This activation-induced cell death requires de novo synthesis of RNA and proteins1–3,
but the actual gene products that provide the death signal have not been identified4–6. We
show here that receptor crosslinking induces Fas ligand and upregulates Fas, and that the
ensuing engagement of Fas by Fas ligand activates the cell-death programme. Cell death,
but not activation, can be selectively prevented by a soluble Fas–immunoglobulin fusion …
Abstract
RECEPTOR crosslinking of T-cell hybridomas induces cell activation followed by apoptosis1–6. This activation-induced cell death requires de novo synthesis of RNA and proteins1–3, but the actual gene products that provide the death signal have not been identified4–6. We show here that receptor crosslinking induces Fas ligand and upregulates Fas, and that the ensuing engagement of Fas by Fas ligand activates the cell-death programme. Cell death, but not activation, can be selectively prevented by a soluble Fas–immunoglobulin fusion protein. Thus, Fas and Fas ligand are the death-gene products, and their interaction accounts for the molecular mechanism of activation-induced T-cell death.
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