ReviewCurrent diabetes reports2014
Self-antigen expression in the peripheral immune system: roles in self-tolerance and type 1 diabetes pathogenesis.
Review in Current diabetes reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 10 citations in OpenAlex.
- Immunotherapy for Type 1 Diabetes: Mechanistic Insights and Impact of Delivery Systems.Current pharmaceutical design · 2025Review
- The role of islet autoantigen-specific T cells in the onset and treatment of type 1 diabetes mellitus.Frontiers in immunology · 2024Review
- Pancreatic draining lymph nodes (PLNs) serve as a pathogenic hub contributing to the development of type 1 diabetes.Cell & bioscience · 2023Review
- Identification of key genes and pathways associated with diabetes of the exocrine pancreas.Medicine · 2022Article
- Tissue-Engineered Stromal Reticula to Study Lymph Node Fibroblastic Reticular Cells in Type I Diabetes.Cellular and molecular bioengineering · 2020Article
- Autoreactive T cells in type 1 diabetes.The Journal of clinical investigation · 2017Review
- Human islets and dendritic cells generate post-translationally modified islet autoantigens.Clinical and experimental immunology · 2016Article
- Inflammation and hyperglycemia mediate Deaf1 splicing in the pancreatic lymph nodes via distinct pathways during type 1 diabetes.Diabetes · 2015Article
Corrections and comments
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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
Type 1 diabetes (T1D) may result from a breakdown in peripheral tolerance that is partially controlled by the ectopic expression of peripheral tissue antigens (PTAs) in lymph nodes. Various subsets of lymph node stromal cells and certain hematopoietic cells play a role in maintaining T cell tolerance. These specialized cells have been shown to endogenously transcribe, process, and present a range of PTAs to naive T cells and mediate the clonal deletion or inactivation of autoreactive cells. During the progression of T1D, inflammation leads to reduced PTA expression in the pancreatic lymph nodes and the production of novel islet antigens that T cells are not tolerized against. These events allow for the escape and activation of autoreactive T cells and may contribute to the pathogenesis of T1D. In this review, we discuss recent findings in this area and propose possible therapies that may help reestablish self-tolerance during T1D.
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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.