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Type I interferons activate apoptosis in a Jurkat cell variant by caspase-dependent and independent mechanisms.

Abstract：

:Although the antiviral actions of interferons (IFNs) are observed in most types of cells, the antiproliferative effects of IFNalpha/beta are variable as are the mechanisms of growth inhibition that may or may not be due to the induction of apoptosis. To understand more about the mechanisms that are responsible for IFNalpha/beta-stimulated apoptosis, we have characterized a new human Jurkat T cell variant named H123 where IFNalpha activates programmed cell death (PCD). No differences in IFNalpha-stimulated, Stat-dependent gene expression were detected between H123 cells and the parental Jurkat cells, which are growth inhibited, but do not undergo apoptosis with IFNalpha. Although IFNalpha stimulates the activity of both caspase 3 and 9 in H123 cells, the general caspase inhibitor Z-VAD only partially reverses the apoptotic actions of IFNalpha. Induction of apoptosis by IFNalpha occurs through a mitochondrial-dependent pathway in H123 cells, as demonstrated by the release of cytochrome C from the mitochondria. Furthermore, IFNalpha treatment of H123 cells stimulates the release of the serine protease HtrA2/Omi from the mitochondria, suggesting that it plays a role in the apoptotic actions of this cytokine. These results provide evidence for a novel type 1 IFN-mediated pathway that regulates apoptosis of T cells through a mitochondrial-dependent and caspase-dependent and independent pathway.

journal_name

Cell Signal

journal_title

Cellular signalling

authors

Gamero AM,Potla R,Sakamoto S,Baker DP,Abraham R,Larner AC

doi

10.1016/j.cellsig.2005.10.008

subject

Has Abstract

pub_date

2006-08-01 00:00:00

pages

1299-308

issue

8

eissn

0898-6568

issn

1873-3913

pii

S0898-6568(05)00281-0

journal_volume

18

pub_type

杂志文章

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