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Jia-Fwu Shyu, Hwai-Shi Wang, Yi-Ming Shyr, Shin-E Wang, Chia-Hsiang Chen, Joo-Shin Tan, Meng-Feng Lin, Po-Shiuan Hsieh, Huey-Kang Sytwu, and Tien-Hua Chen

Introduction Type 1 diabetes is a chronic disease which is characterized by absolute insulin deficiency ( Nerup et al . 1970 , Atkinson 2005 ). Since the discovery of insulin more than 80 years ago and with the advent of glucose monitoring

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J M Mellado-Gil and M Aguilar-Diosdado

Introduction Type 1 diabetes mellitus results from autoimmune T-cell-mediated destruction of insulin-producing pancreatic islet β-cells ( Castaño & Eisenbarth 1990 ). Although the mechanism of this destruction is not completely

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Elizabeth S Barrie, Mels Lodder, Paul H Weinreb, Jill Buss, Amer Rajab, Christopher Adin, Qing-Sheng Mi, and Gregg A Hadley

Introduction Type 1 diabetes is a T cell-mediated autoimmune disease caused by the destruction of insulin-producing β cells of the islets of Langerhans in the pancreas, resulting in a hyperglycemic state. Non-obese diabetic (NOD) mice (NOD

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Astrid Chamson-Reig, Edith J Arany, Kelly Summers, and David J Hill

Introduction Type 1 diabetes originates with the autoimmune-mediated destruction of pancreatic β-cells, and is characterized by a change in cytokine secretion from a helper T-cell (Th) 2 phenotype with relatively low levels of interferon γ (IFNγ

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Subhshri Sahu, David Tosh, and Anandwardhan A Hardikar

Mirbolooki M James Shapiro AM Lakey JR 2006 Stem cell sources for clinical islet transplantation in type 1 diabetes: embryonic and adult stem cells . Medical Hypotheses 67 909 – 913 . Nagaya M Katsuta H Kaneto H Bonner-Weir S Weir GC

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Jon G Mabley, Pal Pacher, Kanneganti G K Murthy, William Williams, Garry J Southan, Andrew L Salzman, and Csaba Szabo

– 6862 . Atkinson MA Leiter EH 1999 The NOD mouse model of type 1 diabetes: as good as it gets? Nature Medicine 5 601 – 604 . Bach J-F 1994 Insulin-dependent diabetes mellitus as an autoimmune disease . Endocrine Reviews 15 516

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Martin Blixt, Bo Niklasson, and Stellan Sandler

( Robertson et al . 2003 ). During the disease progression in type 1 diabetes, the β-cell mass in the pancreatic islets is reduced by immune cell-mediated mechanisms ( Hitchcock et al . 1988 , Bach 1995 , Yoon & Jun 2005 , Knip & Siljander 2008 ). An

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Jung-Hoon Kang, Seo-Yoon Chang, Hyun-Jong Jang, Dong-Bin Kim, Gyeong Ryul Ryu, Seung Hyun Ko, In-Kyung Jeong, Yang-Hyeok Jo, and Myung-Jun Kim

Introduction The main feature of type 1 diabetes mellitus is an autoimmune insulitis, that is, the infiltration of inflammatory cells around the pancreatic islets ( Andre et al . 1996 ). The insulitis is primarily mediated by proinflammatory

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Guofeng Zhang, Hiroki Hirai, Tao Cai, Junnosuke Miura, Ping Yu, Hanxia Huang, Martin R Schiller, William D Swaim, Richard D Leapman, and Abner L Notkins

Introduction IA-2 is a major autoantigen in type 1 diabetes and autoantibodies to it are widely used to identify subjects at high risk of developing type 1 diabetes for entry into therapeutic intervention trials ( Lan et al . 1996

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Min Zhao, Stephanie A Amiel, Michael R Christie, Paolo Muiesan, Parthi Srinivasan, Wendy Littlejohn, Mohamed Rela, Matthew Arno, Nigel Heaton, and Guo Cai Huang

least in the short term, to restore β-cells in Type 1 diabetes by islet transplantation ( Shapiro et al . 2000 ) has renewed interest in attempts to find β-cell surrogates. There are far fewer organ donors than people with diabetes and, at least in its