Premium
Caspase‐Independent Cell Death by Fas Ligation in Human Thymus‐Derived T Cell Line, HPB‐ALL Cells
Author(s) -
Nakayama Junichi,
Ohtsuki Masahiko,
Oda Tomiichiro
Publication year - 2007
Publication title -
microbiology and immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.664
H-Index - 70
eISSN - 1348-0421
pISSN - 0385-5600
DOI - 10.1111/j.1348-0421.2007.tb03987.x
Subject(s) - programmed cell death , biology , apoptosis , fas receptor , caspase , caspase 8 , microbiology and biotechnology , cell culture , dna fragmentation , t cell , jurkat cells , fas ligand , immunology , immune system , biochemistry , genetics
In HPB‐ALL cells, a human thymus‐derived T‐cell line, Fas (CD95)‐mediated cell death was inhibited by about only 50% as a result of treatment with an amount of benzyloxycarbonyl‐Val‐Ala‐Asp‐(O‐methyl)‐CH 2 F (zVAD‐fmk) sufficient to block the caspase activity. Fas‐mediated caspase‐independent cell death was not observed in other lymphoblast cell lines or mouse activated splenocytes, but this type of cell death was observed in mouse and rat thymocytes, the same as for HPB‐ALL cells. This suggests that Fas‐mediated caspase‐independent cell death is a common feature in thymocytes. The signaling pathway of caspase‐independent cell death has not yet been fully elucidated. In HPB‐ALL cells, DNA fragmentation, one of the features of apoptotic cells, did not occur in the caspase‐independent cell death after Fas ligation. On the other hand, this type of cell death and the surface exposure of phosphatidylserine were recovered by pretreatment with geldanamycin, which brought about a decrease in receptor interacting protein (RIP) kinase expression. These results suggested that HPB‐ALL cells have a caspase‐independent RIP kinase‐dependent pathway for Fas ligation.