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Apoptosis in a Fas‐resistant, T‐cell receptor‐sensitive human leukaemic T‐cell clone
Author(s) -
DELEHANTY L. L.,
PAYNE J. A.,
FARROW S. N.,
BROWN R.,
CHAMPION B. R.
Publication year - 1997
Publication title -
immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.297
H-Index - 133
eISSN - 1365-2567
pISSN - 0019-2805
DOI - 10.1111/j.1365-2567.1997.00383.x
Subject(s) - fas receptor , apoptosis , biology , programmed cell death , fas ligand , microbiology and biotechnology , clone (java method) , mutant , cycloheximide , receptor , cell culture , gene , cancer research , genetics
SUMMARY The Fas (CD95) antigen plays a key role in regulating T‐cell activation and survival. We have generated a Fas‐resistant subclone of the human T‐cell leukaemia line, H9, which is still able to undergo apoptosis in response to T‐cell receptor ligation. Molecular analyses revealed that resistance to Fas‐mediated apoptosis was due to a heterozygous mutation in the death domain of the Fas gene which generates a stop codon, and thus encodes a truncated Fas molecule. Fas ligation was able to induce apoptosis in the presence of cycloheximide, indicating that the mutant Fas molecule retained some signalling capability, which is death‐domain independent. These cells will provide a useful tool for dissecting the complexities of Fas signalling pathways.