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J. Exp. Med.,
Volume 186, Number 12, December 15, 1997 2075-2080
By




From the * Howard Hughes Medical Insitute; the TRANCE (tumor necrosis factor [TNF]-related activation-induced cytokine) is a new member of the TNF family that is induced upon T cell receptor engagement and activates c-Jun
N-terminal kinase (JNK) after interaction with its putative receptor (TRANCE-R). In addition, TRANCE expression is restricted to lymphoid organs and T cells. Here, we show that
high levels of TRANCE-R are detected on mature dendritic cells (DCs) but not on freshly
isolated B cells, T cells, or macrophages. Signaling by TRANCE-R appears to be dependent
on TNF receptor-associated factor 2 (TRAF2), since JNK induction is impaired in cells from
transgenic mice overexpressing a dominant negative TRAF2 protein. TRANCE inhibits apoptosis of mouse bone marrow-derived DCs and human monocyte-derived DCs in vitro. The resulting increase in DC survival is accompanied by a proportional increase in DC-mediated T
cell proliferation in a mixed leukocyte reaction. TRANCE upregulates Bcl-xL expression, suggesting a potential mechanism for enhanced DC survival. TRANCE does not induce the proliferation of or increase the survival of T or B cells. Therefore, TRANCE is a new DC-restricted
survival factor that mediates T cell-DC communication and may provide a tool to selectively
enhance DC activity.
Laboratory of Cellular Physiology and Immunology;
and the § Laboratory of Immunology, The Rockefeller University, New York 10021
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