ArticlePloS one2012
Fas-independent T-cell apoptosis by dendritic cells controls autoimmune arthritis in MRL/lpr mice.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 19 citations in OpenAlex.
- Regulatory dendritic cells and their usefulness in mitigating solid organ transplant rejection.Clinical transplantation and research · 2025Review
- A review of immune modulators and immunotherapy in infectious diseases.Molecular and cellular biochemistry · 2024Review
- Periostin in lymph node pre-metastatic niches governs lymphatic endothelial cell functions and metastatic colonization.Cellular and molecular life sciences : CMLS · 2022Article
- Apoptosis, Autophagy, NETosis, Necroptosis, and Pyroptosis Mediated Programmed Cell Death as Targets for Innovative Therapy in Rheumatoid Arthritis.Frontiers in immunology · 2021Review
- Crosstalk between Fas and S1PThe Japanese dental science review · 2019Review
- Article
- Ways Forward for Tolerance-Inducing Cellular Therapies- an AFACTT Perspective.Frontiers in immunology · 2019Review
- Mechanisms of Tolerance Induction by Dendritic CellsFrontiers in immunology · 2018Review
- Harnessing the properties of dendritic cells in the pursuit of immunological tolerance.Biomedical journal · 2017Review
- Tolerance through Education: How Tolerogenic Dendritic Cells Shape Immunity.Frontiers in immunology · 2017Review
- Dual Role of Fas/FasL-Mediated Signal in Peripheral Immune Tolerance.Frontiers in immunology · 2017Review
- Article
- Immune Tolerance Maintained by Cooperative Interactions between T Cells and Antigen Presenting Cells Shapes a Diverse TCR Repertoire.Frontiers in immunology · 2015Article
- Article
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAlthough autoimmunity in MRL/lpr mice occurs due to a defect in Fas-mediated cell death of T cells, the role of Fas-independent apoptosis in pathogenesis has rarely been investigated. We have recently reported that receptor activator of nuclear factor (NF)-κB ligand (RANKL)-activated dendritic cells (DCs) play a key role in the pathogenesis of rheumatoid arthritis (RA) in MRL/lpr mice. We here attempted to establish a new therapeutic strategy with RANKL-activated DCs in RA by controlling apoptosis of peripheral T cells. Repeated transfer of RANKL-activated DCs into MRL/lpr mice was tested to determine whether this had a therapeutic effect on autoimmunity. METHODS AND FINDING: Cellular and molecular mechanisms of Fas-independent apoptosis of T cells induced by the DCs were investigated by in vitro and in vivo analyses. We demonstrated that repeated transfers of RANKL-activated DCs into MRL/lpr mice resulted in therapeutic effects on RA lesions and lymphoproliferation due to declines of CD4(+) T, B, and CD4(-)CD8(-) double negative (DN) T cells. We also found that the Fas-independent T-cell apoptosis was induced by a direct interaction between tumor necrosis factor (TNF)-related apoptosis-inducing ligand-receptor 2 (TRAIL-R2) on T cells and TRAIL on Fas-deficient DCs in MRL/lpr mice.
conclusionThese results strongly suggest that a novel Fas-independent apoptosis pathway in T cells maintains peripheral tolerance and thus controls autoimmunity in MRL/lpr mice.
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