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,
* Division of Neuroimmunology, Department of Neurology, and
Division of Rheumatology/Clinical Immunology, Department of Medicine, Charité University Hospital, and
Deutsches Rheuma-Forschungszentrum, Berlin, Germany
TNF-related apoptosis-inducing ligand (TRAIL), a member of the TNF
superfamily, induces apoptosis in susceptible cells, which can be both
malignant and nontransformed. Despite homologies among the death
ligands, there are great differences between the TRAIL system on the
one hand and the TNF and CD95 systems on the other hand. In particular,
TRAIL-induced apoptosis differs between rodents and man. Studies on
animal models of autoimmune diseases suggested an influence of TRAIL on
T cell growth and effector functions. Because we previously
demonstrated that TRAIL does not induce apoptosis in human
(auto)antigen-specific T cells, we now asked whether TRAIL exhibits
other immunoregulatory properties in these cells. Active TRAIL
inhibited calcium influx through store-operated calcium
release-activated calcium channels, IFN-
/IL-4 production, and
proliferation. These effects were independent of APC, Ag specificity,
and Th differentiation, and no differences were detected between
healthy donors and multiple sclerosis patients. TRAIL affected neither
the expression of the cell cycling inhibitor
p27Kip1 nor the capacity of T cells to produce
IL-2 upon Ag rechallenge, indicating that signaling via TRAIL receptor
does not induce T cell anergy. Instead, the TRAIL-induced
hypoproliferation could be attributed to the down-regulation of the
cyclin-dependent kinase 4, indicating a G1 arrest of the
cell cycle. Thus, although it does not contribute to mechanisms of
peripheral T cell tolerance such as clonal anergy or deletion by
apoptosis, TRAIL can directly inhibit activation of human T cells via
blockade of calcium influx.
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