PMID- 15919368
OWN - NLM
STAT- MEDLINE
DCOM- 20050729
LR  - 20061115
IS  - 0008-8749 (Print)
IS  - 0008-8749 (Linking)
VI  - 231
IP  - 1-2
DP  - 2004 Sep-Oct
TI  - TRANCE counteracts FasL-mediated apoptosis of murine bone marrow-derived 
      dendritic cells.
PG  - 40-8
AB  - Dendritic cells (DCs) are the most potent APCs known to date. Despite their 
      potency, DCs are short-lived. During the course of an immune response, DCs 
      interact with cognate T cells, which upon activation express both DC survival and 
      pro-apoptotic factors. This raises the question how DC longevity is regulated by 
      these signals. In this study, we have assessed the roles of FasL (CD95L) and 
      tumor necrosis factor-related activation-induced cytokine (TRANCE) in regulating 
      the survival of murine bone marrow-derived DCs (BMDCs). We have shown for the 
      first time that TRANCE protects DCs from FasL-mediated apoptosis, and that the 
      quantitative balance between TRANCE and FasL can modulate BMDC survival in vitro. 
      In addition, by quantifying adoptively transferred BMDCs in draining lymph nodes 
      (LNs), we have shown that treating DCs with FasL prior to the transfer decreases 
      the quantity of donor DCs capable of migrating to the LN, presumably due to 
      FasL-mediated apoptosis of donor DCs in vivo. Furthermore, we have shown that 
      TRANCE can counteract FasL and reverse such decrease. Taken together, these 
      results suggest that the interplay between FasL and TRANCE play a role in 
      regulating the survival of DCs.
FAU - Chen, Aoshuang
AU  - Chen A
AD  - Department of Biomedical Sciences, College of Medicine, University of Illinois, 
      1601 Parkview Avenue, Rockford, IL 61107, USA. aoshuang@uic.edu
FAU - Xu, Hongwu
AU  - Xu H
FAU - Choi, Yongwon
AU  - Choi Y
FAU - Wang, Bin
AU  - Wang B
FAU - Zheng, Guoxing
AU  - Zheng G
LA  - eng
PT  - Journal Article
DEP - 20041225
PL  - Netherlands
TA  - Cell Immunol
JT  - Cellular immunology
JID - 1246405
RN  - 0 (Carrier Proteins)
RN  - 0 (Fas Ligand Protein)
RN  - 0 (Fasl protein, mouse)
RN  - 0 (Membrane Glycoproteins)
RN  - 0 (RANK Ligand)
RN  - 0 (Receptor Activator of Nuclear Factor-kappa B)
RN  - 0 (Recombinant Proteins)
RN  - 0 (Tnfrsf11a protein, mouse)
RN  - 0 (Tnfsf11 protein, mouse)
SB  - IM
MH  - Animals
MH  - *Apoptosis
MH  - Bone Marrow Cells/*cytology
MH  - CD4-Positive T-Lymphocytes/metabolism
MH  - Carrier Proteins/*metabolism
MH  - *Cell Differentiation
MH  - Cells, Cultured
MH  - Dendritic Cells/*cytology/*metabolism
MH  - Fas Ligand Protein
MH  - Lymph Nodes/cytology/metabolism
MH  - Membrane Glycoproteins/*metabolism
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - Mice, Inbred C57BL
MH  - RANK Ligand
MH  - Receptor Activator of Nuclear Factor-kappa B
MH  - Recombinant Proteins/metabolism
MH  - Spleen/cytology/metabolism
EDAT- 2005/05/28 09:00
MHDA- 2005/07/30 09:00
CRDT- 2005/05/28 09:00
PHST- 2004/06/16 00:00 [received]
PHST- 2004/11/09 00:00 [revised]
PHST- 2004/11/16 00:00 [accepted]
PHST- 2005/05/28 09:00 [pubmed]
PHST- 2005/07/30 09:00 [medline]
PHST- 2005/05/28 09:00 [entrez]
AID - S0008-8749(04)00183-2 [pii]
AID - 10.1016/j.cellimm.2004.11.005 [doi]
PST - ppublish
SO  - Cell Immunol. 2004 Sep-Oct;231(1-2):40-8. doi: 10.1016/j.cellimm.2004.11.005. 
      Epub 2004 Dec 25.