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Blood, 15 April 2001, Vol. 97, No. 8, pp. 2205-2212
CHEMOKINES
The C-class chemokine lymphotactin costimulates the apoptosis
of human CD4+ T cells
Chantal Cerdan,
Elisabeth Devilard,
Luc Xerri, and
Daniel Olive
From the National Institute of Health and Medical
Research, University of Méditerranée and Department of
Hematopathology, Institut Paoli-Calmettes, Marseille, France.
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  -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.
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