ArticleThe review of diabetic studies : RDS2006
Death pathways in T cell homeostasis and their role in autoimmune diabetes.
Article in The review of diabetic studies : RDS, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 27 citations in OpenAlex.
- Transcriptomics analysis reveals potential mechanisms underlying mitochondrial dysfunction and T cell exhaustion in astronauts' blood cells in space.Frontiers in immunology · 2024Article
- Immune Modulation Using Extracellular Vesicles Encapsulated with MicroRNAs as Novel Drug Delivery Systems.International journal of molecular sciences · 2022Review
- PD-1 expression is upregulated on adapted T cells in experimental autoimmune encephalomyelitis but is not required to maintain a hyporesponsive state.European journal of immunology · 2019Article
- Mechanisms of Tolerance Induction by Dendritic CellsFrontiers in immunology · 2018Review
- Defective expression of apoptosis-related molecules in multiple sclerosis patients is normalized early after autologous haematopoietic stem cell transplantation.Clinical and experimental immunology · 2017Article
- Mesenchymal Stem Cells Secretory Responses: Senescence Messaging Secretome and Immunomodulation Perspective.Frontiers in genetics · 2017Review
- Survival of autoreactive T lymphocytes by microRNA-mediated regulation of apoptosis through TRAIL and Fas in type 1 diabetes.Genes and immunity · 2016Article
- Macroautophagy inhibition maintains fragmented mitochondria to foster T cell receptor-dependent apoptosis.The EMBO journal · 2016Article
- T-cell death following immune activation is mediated by mitochondria-localized SARM.Cell death and differentiation · 2013Article
- Up-regulation of fas and fasL pro-apoptotic genes expression in type 1 diabetes patients after autologous haematopoietic stem cell transplantation.Clinical and experimental immunology · 2012Article
- Immune profiling by multiple gene expression analysis in patients at-risk and with type 1 diabetes.Clinical immunology (Orlando, Fla.) · 2011Article
- Gene therapy in diabetes.Self/nonself · 2010Article
- Mitochondrial nutrients improve immune dysfunction in the type 2 diabetic Goto-Kakizaki rats.Journal of cellular and molecular medicine · 2009Article
- Mitochondrial DNA variants in the pathogenesis of type 2 diabetes - relevance of asian population studies.The review of diabetic studies : RDS · 2009Article
- The cross-regulatory relationship between human dendritic and regulatory T cells and its role in type 1 diabetes mellitus.The review of diabetic studies : RDS · 2007Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
T cell apoptosis is a process necessary for central and peripheral tolerance. It ensures the proper removal of autoreactive T cells during thymic development as well as T cell homeostasis and the downregulation of immune responses against antigens in the periphery. Thus it is essential for the prevention of autoimmunity. Apoptotic pathways can be triggered by intrinsic (mitochondria-based) and extrinsic (receptor-based) stimuli. Both pathways involve a cascade of proteolytic enzymes called caspases whose activation commits the cell to death. In the periphery, autoreactive lymphocytes can be silenced by developmental arrest (anergy), or deleted by programmed cell death (apoptosis) through receptor-based activation-induced cell death (AICD). Central tolerance seems to rely more heavily on the mitochondria-based, T cell receptor (TCR)-stimulated apoptotic pathway, since thymocytes lacking the pro-apoptotic Bcl-2 family member Bim are resistant to TCR-induced apoptosis. Furthermore, defects in the intrinsic pathway of apoptosis may impair clonal deletion of autoreactive T cells. Several animal models exist in which impaired apoptosis results in autoimmunity. Here, we discuss data that suggest defects in T cell apoptosis in type 1 diabetes mellitus.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.