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TRANCE (tumor necrosis factor [TNF]-related activation-induced cytokine), a new TNF family member predominantly expressed in T cells, is a dendritic cell-specific survival factor.

Wong BR, Josien R, Lee SY, Sauter B, Li HL, Steinman RM, Choi Y - J. Exp. Med. (1997)

Bottom Line: 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.The resulting increase in DC survival is accompanied by a proportional increase in DC-mediated T cell proliferation in a mixed leukocyte reaction.TRANCE does not induce the proliferation of or increase the survival of T or B cells.

View Article: PubMed Central - PubMed

Affiliation: Laboratory of Immunology, The Rockefeller University, New York 10021, USA.

ABSTRACT
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.

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TRANCE does  not induce the proliferation of B  or T cells. Triplicate wells of 2 ×  104 purified B cells were cultured  in complete medium in the presence of increasing doses of soluble  TRANCE or CD40L in flat-bottomed 96-well plates. 105 purified  T cells were cultured in complete  medium containing Con A (2.5  μg/ml) in the presence of increasing doses of soluble TRANCE.  [3H]thymidine incorporation was  assessed after 2 d of culture.
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Figure 4: TRANCE does not induce the proliferation of B or T cells. Triplicate wells of 2 × 104 purified B cells were cultured in complete medium in the presence of increasing doses of soluble TRANCE or CD40L in flat-bottomed 96-well plates. 105 purified T cells were cultured in complete medium containing Con A (2.5 μg/ml) in the presence of increasing doses of soluble TRANCE. [3H]thymidine incorporation was assessed after 2 d of culture.

Mentions: Expression of high levels of the TRANCE-R appeared restricted to DCs by FACS® analysis. However, we found that TRANCE could activate JNK in thymocytes (22), suggesting that FACS® analysis might lack the sensitivity to detect low levels of receptor. To further examine the specificity of TRANCE for DCs, we tested its ability to induce B cell proliferation or survival, two functions mediated by CD40L. Recombinant hCD8-TRANCE, tested for its antiapoptotic function in BMDCs, could not stimulate B cell proliferation (Fig. 4), nor could it activate JNK activation (22). In contrast, CD40L efficiently stimulated B cell proliferation in a dose-dependent manner (Fig. 4). Finally, TRANCE could not prevent the spontaneous apoptosis of B and T cells as assessed by propidium iodide uptake (data not shown). Therefore, functionally, TRANCE appears to exhibit different cellular specificities and functions when compared to CD40L.


TRANCE (tumor necrosis factor [TNF]-related activation-induced cytokine), a new TNF family member predominantly expressed in T cells, is a dendritic cell-specific survival factor.

Wong BR, Josien R, Lee SY, Sauter B, Li HL, Steinman RM, Choi Y - J. Exp. Med. (1997)

TRANCE does  not induce the proliferation of B  or T cells. Triplicate wells of 2 ×  104 purified B cells were cultured  in complete medium in the presence of increasing doses of soluble  TRANCE or CD40L in flat-bottomed 96-well plates. 105 purified  T cells were cultured in complete  medium containing Con A (2.5  μg/ml) in the presence of increasing doses of soluble TRANCE.  [3H]thymidine incorporation was  assessed after 2 d of culture.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC2199171&req=5

Figure 4: TRANCE does not induce the proliferation of B or T cells. Triplicate wells of 2 × 104 purified B cells were cultured in complete medium in the presence of increasing doses of soluble TRANCE or CD40L in flat-bottomed 96-well plates. 105 purified T cells were cultured in complete medium containing Con A (2.5 μg/ml) in the presence of increasing doses of soluble TRANCE. [3H]thymidine incorporation was assessed after 2 d of culture.
Mentions: Expression of high levels of the TRANCE-R appeared restricted to DCs by FACS® analysis. However, we found that TRANCE could activate JNK in thymocytes (22), suggesting that FACS® analysis might lack the sensitivity to detect low levels of receptor. To further examine the specificity of TRANCE for DCs, we tested its ability to induce B cell proliferation or survival, two functions mediated by CD40L. Recombinant hCD8-TRANCE, tested for its antiapoptotic function in BMDCs, could not stimulate B cell proliferation (Fig. 4), nor could it activate JNK activation (22). In contrast, CD40L efficiently stimulated B cell proliferation in a dose-dependent manner (Fig. 4). Finally, TRANCE could not prevent the spontaneous apoptosis of B and T cells as assessed by propidium iodide uptake (data not shown). Therefore, functionally, TRANCE appears to exhibit different cellular specificities and functions when compared to CD40L.

Bottom Line: 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.The resulting increase in DC survival is accompanied by a proportional increase in DC-mediated T cell proliferation in a mixed leukocyte reaction.TRANCE does not induce the proliferation of or increase the survival of T or B cells.

View Article: PubMed Central - PubMed

Affiliation: Laboratory of Immunology, The Rockefeller University, New York 10021, USA.

ABSTRACT
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.

Show MeSH
Related in: MedlinePlus