Attacking the source: anti-PDX-1 responses in type 1 diabetes
- PMID: 20038945
- PMCID: PMC3756500
- DOI: 10.1038/labinvest.2009.121
Attacking the source: anti-PDX-1 responses in type 1 diabetes
Abstract
Type 1 diabetes (T1D) develops as a consequence of abnormal responses against several self-antigens, eventually leading to the autoimmune attack and destruction of the insulin-producing beta cells in the pancreas. In this issue of Laboratory Investigation, Li et al propose the transcription factor Pancreatic and duodenal homeobox 1 (PDX-1) as a T1D autoantigen by demonstrating autoreactivity to this pancreas-specific protein in both the NOD mouse model and patients with T1D. Because of the known roles of PDX-1 in pancreatic development as well as beta cell maintenance and function, targeting of PDX-1 expressing cells may result in the elimination of not only beta cells but also the progenitor cells required for regeneration of insulin-producing cells.
Comment on
-
Pancreatic duodenal homeobox 1 protein is a novel beta-cell-specific autoantigen for type I diabetes.Lab Invest. 2010 Jan;90(1):31-9. doi: 10.1038/labinvest.2009.116. Epub 2009 Nov 9. Lab Invest. 2010. PMID: 19901909 Free PMC article.
References
-
- Eisenbarth GS, Jeffrey J. The natural history of type 1A diabetes. Arquivos brasileiros de endocrinologia e metabologia. 2008;52:146–155. - PubMed
-
- Pietropaolo M, Yu S, Libman IM, et al. Cytoplasmic islet cell antibodies remain valuable in defining risk of progression to type 1 diabetes in subjects with other islet autoantibodies. Pediatr Diabetes. 2005;6:184–192. - PubMed
-
- Verge CF, Gianani R, Kawasaki E, et al. Prediction of type I diabetes in first-degree relatives using a combination of insulin, GAD, and ICA512bdc/IA-2 autoantibodies. Diabetes. 1996;45:926–933. - PubMed
-
- Wang J, Miao D, Babu S, et al. Prevalence of autoantibody-negative diabetes is not rare at all ages and increases with older age and obesity. J Clin Endocrinol Metab. 2007;92:88–92. - PubMed
Publication types
MeSH terms
Substances
Grants and funding
LinkOut - more resources
Full Text Sources
Medical
Research Materials
