Abstract:
:Clonal expansion of activated T cells is controlled by homeostatic mechanisms leading to cell death of a large proportion of the cells. The CD3/TcR pathway induces cell death, mostly when triggered in the absence of costimulatory signal. The unique T cell-specific chemokine of the C class, lymphotactin (Lptn), has recently been shown to inhibit the production of Th1-type lymphokines in human CD4(+) T cells. The present study shows the ability of Lptn to costimulate the death of CD4(+) T lymphocytes triggered through CD3/TCR. The Lptn-mediated increased cell death exhibited characteristic features of apoptosis, as mainly determined by DNA fragmentation and exposure of an apoptotic-specific mitochondrial antigen. This apoptosis was dependent on Fas/FasL signaling, was not rescued by addition of interleukin 2, and proceeded with a predominant processing of both initiator procaspase-9 and effector procaspase-7. These caspase activities were further evidenced by specific cleavage of poly(ADP-ribose) polymerase (PARP) and CD3/TCR zeta-chain, but not DNA fragmentation factor (DFF45). This study demonstrates that the functional repertoire of Lptn in the regulation of human CD4(+) T-lymphocyte activation includes the ability to costimulate apoptosis.
journal_name
Bloodjournal_title
Bloodauthors
Cerdan C,Devilard E,Xerri L,Olive Ddoi
10.1182/blood.v97.8.2205subject
Has Abstractpub_date
2001-04-15 00:00:00pages
2205-12issue
8eissn
0006-4971issn
1528-0020journal_volume
97pub_type
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