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Blood, Vol. 96 No. 2 (July 15), 2000:
pp. 420-428
The C-class chemokine, lymphotactin, impairs the induction of
Th1-type lymphokines in human CD4+ T cells
Chantal Cerdan,
Edgar Serfling, and
Daniel Olive
From the National Institute of Health and Medical Research,
University of Méditerranée, Marseille, France; Department
of Molecular Pathology, Institute of Pathology, Würzburg,
Germany.
Chemokines are involved in the regulation of leukocyte migration and
for some of them, T-cell costimulation. To date, the only direct
property of lymphotactin (Lptn), the unique member of the C class of
chemokines, consists of T-cell chemoattraction. This report describes a
novel function for Lptn in human T-lymphocyte biology, by demonstrating
the direct ability of Lptn to both inhibit and costimulate
CD4+ and CD8+ T-cell activation,
respectively. Lptn but not RANTES inhibited CD4+ T-cell
proliferation, through a decreased production of Th1 (interleukin [IL]-2, interferon [IFN]- ) but not Th2 (IL-4, IL-13)
lymphokines, and decreased IL-2R expression. Transfections in Jurkat
cells showed a Lptn-mediated transcriptional down-regulation of
gene-promoter activities specific for Th1-type lymphokines, as well as
of nuclear factor of activated T cells (NF-AT) but not AP-1 or
NF-KB enhancer activities. This suppressive action of
Lptn could be compensated by overexpression of NF-ATc but not NF-ATp.
CD4+ T-cell proliferation was completely restored by
exogenous IL-2 or reversed by pertussis toxin, wortmannin, and
genistein, suggesting the involvement of multiple partners in Lptn
signaling. In contrast to CD4+ cells, Lptn exerted a
potent costimulatory activity on CD8+ T-cell
proliferation and IL-2 secretion. These data provide important insights
into the role of Lptn in differential regulation of normal human T-cell
activation and its possible implication in immune response disorders.
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