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Rosalia C M Simmen, Dustin M Brown, Charles M Quick, Iad Alhallak, Tyler Rose, Shi J Liu, and Angela S Kelley

Introduction Type 1 diabetes mellitus (T1DM) is an autoimmune disease, resulting from the destruction of insulin-producing β-cells of the pancreatic islets of Langerhans, which leads to a state of hypoinsulinemia and hyperglycemia. In 2015, 1

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Yoko Yagishita, Akira Uruno, Dionysios V Chartoumpekis, Thomas W Kensler, and Masayuki Yamamoto

Introduction Type 1 diabetes is caused by destruction or dysfunction of insulin-producing pancreatic β-cells, and its incidence is increasing in the modern world ( Tuomilehto 2013 ). Protecting β-cells from inflammation and destruction is an

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

reduction in insulin-producing pancreatic β-cells has been considered to be one of the key factors in the development of diabetes, particularly type 1 diabetes ( Yoon & Jun 2001 , Mandrup-Poulsen 2003 ). In type 1 diabetes, autoimmune destruction of the

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James C Needell, Madalyn N Brown, and Danny Zipris

Introduction Type 1 diabetes (T1D) is a proinflammatory progressive disease thought to be triggered by both genetic and environmental factors ( Atkinson et al . 2014 ). There is evidence supporting the notion that viruses are key players in

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Jennifer A Crookshank, Daniel Serrano, Gen-Sheng Wang, Christopher Patrick, Baylie S Morgan, Marie-France Paré, and Fraser W Scott

Introduction Type 1 diabetes (T1D) occurs in a small subset of genetically susceptible individuals whose immune systems destroy most of the pancreatic β-cells. Recent studies suggest that T1D begins in humans at a very early age, but the

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Gemma Llauradó, Victòria Ceperuelo-Mallafré, Carme Vilardell, Rafael Simó, Pilar Gil, Albert Cano, Joan Vendrell, and José-Miguel González-Clemente

Introduction Cardiovascular disease is the major cause of mortality in type 1 diabetes ( Libby et al . 2005 ). Diabetes mellitus results in an accelerated arteriosclerotic process, which is not fully explained by classical cardiovascular risk

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Wu Luo, Lan Huang, Jingying Wang, Fei Zhuang, Zheng Xu, Haimin Yin, Yuanyuan Qian, Guang Liang, Chao Zheng, and Yi Wang

hoc test when comparing non-parametric data. Differences were considered to be significant at P  < 0.05. Results Inhibition of EGFR-STAT3 signaling improves cardiac function in mouse model of STZ-induced type 1 diabetes We tested the

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Anna Krook

Peripheral insulin resistance is characteristic not only for subjects with type 2 diabetes, but a clinically relevant finding also in subjects with type 1 diabetes ( Yki-Järvinen et al . 1987 , Rossetti et al . 1990 , Bingley et al . 2008

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Marika Bogdani, Angela M Henschel, Sanjay Kansra, Jessica M Fuller, Rhonda Geoffrey, Shuang Jia, Mary L Kaldunski, Scott Pavletich, Simon Prosser, Yi-Guang Chen, Åke Lernmark, and Martin J Hessner

Introduction Type 1 diabetes (T1D) is an autoimmune disease characterized by immunocyte infiltration of the pancreatic islets (insulitis) and destruction of the insulin-secreting β cells. Diabetes in the biobreeding (BB) rat exhibits many

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L Monetini, F Barone, L Stefanini, A Petrone, T Walk, G Jung, R Thorpe, P Pozzilli, and MG Cavallo

Enhanced cellular immune response to bovine beta-casein has been reported in patients with type 1 diabetes. In this study we aimed to establish beta-casein-specific T cell lines from newly diagnosed type 1 diabetic patients and to characterise these cell lines in terms of phenotype and epitope specificity. Furthermore, since sequence homologies exist between beta-casein and putative beta-cell autoantigens, reactivity to the latter was also investigated. T cell lines were generated from the peripheral blood of nine recent onset type 1 diabetic patients with different HLA-DQ and -DR genotypes, after stimulation with antigen pulsed autologous irradiated antigen presenting cells (APCs) and recombinant human interleukin-2 (rhIL-2). T cell line reactivity was evaluated in response to bovine beta-casein, to 18 overlapping peptides encompassing the whole sequence of beta-casein and to beta-cell antigens, including the human insulinoma cell line, CM, and a peptide from the beta-cell glucose transporter, GLUT-2. T cell lines specific to beta-casein could not be isolated from HLA-matched and -unmatched control subjects. beta-Casein T cell lines reacted to different sequences of the protein, however a higher frequency of T cell reactivity was observed towards the C-terminal portion (peptides B05-14, and B05-17 in 5/9 and 4/9 T cell lines respectively). Furthermore, we found that 1 out of 9 beta-casein-specific T cell lines reacted also to the homologous peptide from GLUT-2, and that 3 out of 4 of tested cell lines reacted also to extracts of the human insulinoma cell line, CM. We conclude that T cell lines specific to bovine beta-casein can be isolated from the peripheral blood of patients with type 1 diabetes; these cell lines react with multiple and different sequences of the protein particularly towards the C-terminal portion. In addition, reactivity of beta-casein T cell lines to human insulinoma extracts and GLUT-2 peptide was detected, suggesting that the potential cross-reactivity with beta-cell antigens deserves further investigation.