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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

-deficient hosts successfully traffic to the general graft site but completely fail to accumulate within the islet allograft itself ( Feng et al . 2002 ). This histological picture is strikingly similar to the peri-insulitis stage in the development of

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

the islet and these cells are cytotoxic to islet β-cells in part by producing cytokines and free radicals ( Rabinovitch & Suarez-Pinzon 1998 ). It has been proposed that the insulitis lesion is β-cell destructive when Th1 cytokines (IL-12, interferon

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Chun Zeng, Xin Yi, Danny Zipris, Hongli Liu, Lin Zhang, Qiaoyun Zheng, Krishnamurthy Malathi, Ge Jin, and Aimin Zhou

lymphocytes, around the islets in NOD mice starts at 3–4 weeks of age, causing insulitis ( Solomon & Sarvetnick 2004 , Anderson & Bluestone 2005 ). It has been well demonstrated that CD4 + and CD8 + T cells play an important role in the onset of type 1

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Richard W Nelson and Claudia E Reusch

involved in the etiopathogenesis of diabetes mellitus in dogs and cats Dog Cat Genetics Islet amyloidosis Immune-mediated insulitis Obesity Pancreatitis Pancreatitis Obesity Concurrent hormonal disease Concurrent hormonal disease  Hyperadrenocorticism

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E Kim, S Sohn, M Lee, J Jung, R D Kineman, and S Park

. Like AA & Rossini AA 1976 Streptozotocin-induced pancreatic insulitis: new model of diabetes mellitus. Science 193 415 –417. Liu K , Paterson AJ, Konrad RJ, Parlow AF, Jimi S, Roh M, Chin E Jr & Kudlow JE 2002

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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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Simon C Lee, Christine A Robson-Doucette, and Michael B Wheeler

buffer) only. Mice were maintained for 14 days after the start of treatment to allow animals to reach and surpass the peak incidence of β-cell apoptosis, which occurs at approximately day 11 when insulitis is maximal ( O'Brien et al . 1996 ). Mice were

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C M Allan, Y Wang, M Jimenez, B Marshan, J Spaliviero, P Illingworth, and D J Handelsman

, Nakazawa T, Yonekura H, Takasawa S & Okamoto H 1998 Transgenic mice overexpressing type 2 nitric-oxide synthase in pancreatic beta cells develop insulin-dependent diabetes without insulitis. Journal of Biological Chemistry 273 2493 –2496

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J M Mellado-Gil and M Aguilar-Diosdado

-κB-dependent apoptosis in pancreatic β-cells: potential mechanisms for viral-induced insulitis and β-cell death in type 1 diabetes mellitus. Endocrinology 143 1225 –1234. Loweth AC , Williams GT, James RF, Scarpello JH & Morgan NG 1998

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Daniel Nyqvist, Göran Mattsson, Martin Köhler, Varda Lev-Ram, Arne Andersson, Per-Ola Carlsson, Astrid Nordin, Per-Olof Berggren, and Leif Jansson

. There were no signs of insulitis or any other type of inflammatory process in the transgenic mice. In vitro studies of islets The islet DNA content of C57BL/6 and YC-3.0 mice was similar (21.5 ± 0.6 vs 20.8 ± 0.2 μg