Genetics, pathogenesis and clinical interventions in type 1 diabetes

By J. Bluestone, K. Herold, G. Eisenbarth. Nature, 2010

1,267 citations recorded by the source corpus.

Type 1 diabetes is an autoimmune disorder afflicting millions of people worldwide. Once diagnosed, patients require lifelong insulin treatment and can experience numerous disease-associated complications. The last decade has seen tremendous advances in elucidating the causes and treatment of the disease based on extensive research both in rodent models of spontaneous diabetes and in humans. Integrating these advances has led to the recognition that the balance between regulatory and effector T cells determines disease risk, timing of disease activation, and disease tempo. Here we describe current progress, the challenges ahead and the new interventions that are being tested to address the unmet need for preventative or curative therapies.

Subfields: Endocrinology, Diabetes and Metabolism, Genetics, Surgery

View Paper: https://www.semanticscholar.org/paper/d68d339239a4964937c04c8b19dc5fe15cfbacdf

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Endocrinology, Diabetes and Metabolism

1. R. Kaufman

In Genetics

1. J. Buckner
2. R. Kaufman
3. Lihua Julie Zhu
4. J. Bluestone

In Surgery

1. R. Kaufman
2. J. Buckner
3. J. Bluestone
4. F. Urano
5. C. M. Oslowski
6. J. Malhotra

Citations in the corpus

• Thioredoxin-interacting protein mediates ER stress-induced β cell death through initiation of the inflammasome (2012, background): “Cel an absolute deficiency of insulin (Atkinson et al., 2011; Bluestone et al., 2010).”
• Type 1 diabetes immunotherapy using polyclonal regulatory T cells (2015, background): “Type 1 diabetes (T1D) is an autoimmune disease that occurs in genetically susceptible individuals, influenced by the environment and stochastic events (1).”
• Super-enhancers in the control of cell identity and disease. (2013, neutral): “Type 1 diabetes is caused by T-cell mediated autoimmune destruction of pancreatic beta cells, and much of the genetic variation implicated in type 1 diabetes is associated with major histocompatibility antigens, interleukin-2 signaling, T-cell receptor signaling and interferon signaling (Bluestone e”
• IL-6 in inflammation, autoimmunity and cancer (2020, background): “…senescent cells themselves are critically involved in T1D and T2D, and the deletion of senescent beta cells prevents diabetes (57, 298), indicating that even in T1D in which tissue-specific T cells are involved (299–301), local initiators originating from senescent beta cells play critical roles.”