TRANCE counteracts FasL-mediated apoptosis of murine bone marrow-derived dendritic cells
Abstract
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.
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RANK activation of Langerhans cells by UV can induce pro-survival and anti-apoptotic signals due to upregulation of Bcl-xL, leading to generation of regulatory T cells.
“Intriguingly, receptor activator of NF-κB (RANK) activation of LCs by UV can induce the pro-survival and anti-apoptotic signals due to the upregulation of Bcl-xL, leading to the generation of regulatory T cells.”
From Molecular Mechanisms of UV-Induced Apoptosis and Its Effects on Skin Residential Cells: The Implication in UV-Based Phototherapy (2013) · cites this paper as [67]
A well-characterized consequence of RANK activation on Langerhans cells is an anti-apoptotic signal caused by the upregulation of Bcl-xL.
“A well-characterized consequence of RANK activation on LCs is an anti-apoptotic signal caused by the upregulation of Bcl-xL [67–69].”
From Molecular Mechanisms of UV-Induced Apoptosis and Its Effects on Skin Residential Cells: The Implication in UV-Based Phototherapy (2013) · cites this paper as [67]
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Ma, D. Y., & Clark, E. A. (2009) · Seminars in Immunology · doi:10.1016/j.smim.2009.05.010 · Cited by 446 · see citing works
Lee, C.-H., Wu, S.-B., Hong, C.-H., Yu, H.-S., & Wei, Y.-H. (2013) · International Journal of Molecular Sciences · doi:10.3390/ijms14036414 · Cited by 271 · see citing works
- Authors
- Chen, A., Xu, H., Choi, Y., Wang, B., & Zheng, G.
- Affiliations
- University of Illinois Chicago, Rockford campus (US)
- University of Pennsylvania (US)
- China Agricultural University (CN)
- Corresponding author
- Chen, Aoshuang
- Venue
- Cellular Immunology
- Publisher
- Elsevier BV
- Published
- 2004-09
- Volume
- 231
- Issue
- 1-2
- Pages
- 40-48
- ISSN
- 0008-8749 (ISSN-L)
- OpenAlex
- W2018537198
- Cited by
- 15
- References
- 0
- Citations by year
- 2024: 1 · 2022: 1 · 2016: 1 · 2015: 1 · 2013: 2 · 2012: 2
- FWCI
- 0.36
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Cellular Immunology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Life Sciences › Immunology and Microbiology › Immunology › Immunotherapy and Immune Responses
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Keywords
- trance, Fas ligand, dendritic cell apoptosis, dendritic cell survival, bone marrow-derived dendritic cells, dendritic cell migration, draining lymph nodes, T cell activation, antigen-presenting cells, Fas signaling
- MeSH terms
- Animals, Bone Marrow Cells, Carrier Proteins, Cell Differentiation, Cells, Cultured, Dendritic Cells, Lymph Nodes, Membrane Glycoproteins, Mice, Inbred BALB C, Mice, Inbred C57BL, Recombinant Proteins, Spleen, CD4-Positive T-Lymphocytes, Apoptosis, Mice, Fas Ligand Protein, RANK Ligand, Receptor Activator of Nuclear Factor-kappa B
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