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Caspase‐8 regulates a form of death that is distinct from apoptosis in T cells
Author(s) -
Ch'en Irene L,
Beisner Daniel R,
Degterev Alexei,
Lynch Candace,
Yuan Junying,
Hoffmann Alexander,
Hedrick Stephen M
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.2_supplement.369
Subject(s) - apoptosis , programmed cell death , microbiology and biotechnology , caspase , caspase 8 , t cell , biology , caspase 3 , immune system , caspase 2 , chemistry , immunology , biochemistry
Caspase‐8 is a cysteine protease that is an essential initiator of death receptor‐mediated apoptosis. Paradoxically, it has been shown that T cells require Caspase‐8 for proliferation following antigenic or mitogenic stimulation. We have generated a T cell‐specific conditional deletion of Caspase‐8, and found that deletion of Caspase‐8 causes profound hypo‐proliferation in T cells, both in vitro and in an immune response to LCMV. Further characterization has revealed that T cells deficient in Caspase‐8 do not have a defect in cell cycle progression, but rather experience an abnormally high rate of cell death that does not exhibit hallmarks of classic apoptosis. Contrary to published work, the loss of cell viability does not result from a defect in NFkB activation. Instead, we find Caspase‐8 deficient T cells die by an alternative form of cell death.