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Elisabet Estil.les, Noèlia Téllez, Joan Soler, and Eduard Montanya

inhibit the expression of IGFs in several cell types ( Ilvemarski et al . 1993 , Martin et al . 1993 , Lin et al . 1994 ), and a reduction in IGF2 immunoreactivity has been found in islet cells undergoing insulitis, suggesting that cytokines may

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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

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C Giuliani, M Saji, I Bucci, G Fiore, M Liberatore, D S Singer, F Monaco, L D Kohn, and G Napolitano

-expression of TLR-3 signals to both islet cells and thyrocytes in insulitis/diabetes and Hashimoto’s thyroiditis are striking, given the importance of insulin/IGF-I to regulate islet- and thyroid cell-specific functions. We are investigating whether MHC class I

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A K Katakam, G Chipitsyna, Q Gong, A R Vancha, J Gabbeta, and H A Arafat

high glucose and glucosamine-responsive elements in the OPN promoter ( Asaumi et al. 2003 ). β-Cell destructive insulitis in type I ( Rabinovitch 1998 ) and streptozotocin (STZ)-induced experimental diabetes ( Lukic et al. 1998 , Rydgren

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Craig S Nunemaker, H Grace Chung, Gretchen M Verrilli, Kathryn L Corbin, Aditi Upadhye, and Poonam R Sharma

Boni-Schnetzler M Ehses JA Faulenbach M Donath MY 2008 Insulitis in type 2 diabetes . Diabetes, Obesity & Metabolism 10 ( Suppl 4 ) 201 – 204 . ( doi:10.1111/j.1463-1326.2008.00950.x ) Burke SJ Lu D Sparer TE Masi T Goff MR

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Maria Petropavlovskaia, Julia Makhlin, John Sampalis, and Lawrence Rosenberg

-cells from inflammatory, cytokine-induced cell death, both in vitro and in vivo ( Choi et al. 2004 ). Transgenic mice overexpressing IL-6 in β cells may or may not develop insulitis but they do not develop pancreatitis or diabetes ( Campbell et al

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K Goosse, T Bouckenooghe, M Balteau, B Reusens, and C Remacle

found in higher concentration in type-1 diabetes patients ( Nicoletti et al . 2002 , Cipollone et al . 2005 ), where they participate in the recruitment and activation of lymphocytes and macrophages implicated in insulitis ( Atkinson & Wilson 2002

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José Edgar Nicoletti-Carvalho, Tatiane C Araújo Nogueira, Renata Gorjão, Carla Rodrigues Bromati, Tatiana S Yamanaka, Antonio Carlos Boschero, Licio Augusto Velloso, Rui Curi, Gabriel Forato Anhê, and Silvana Bordin

-cells exposed to long-chain saturated and monounsaturated fatty acids . Journal of Endocrinology 197 553 – 563 . DiCosmo BF Picarella D Flavell RA 1994 Local production of human IL-6 promotes insulitis but retards the onset of insulin

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Manuel C Lemos, Brian Harding, Anita A C Reed, Jeshmi Jeyabalan, Gerard V Walls, Michael R Bowl, James Sharpe, Sarah Wedden, Julie E Moss, Allyson Ross, Duncan Davidson, and Rajesh V Thakker

molecular assessments to investigate autoimmune insulitis in type 1 diabetes mellitus ( Alanentalo et al . 2008 ). In summary, our study, which has demonstrated the effects of genetic background on the phenotypes of embryonic lethality and neural tube

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Gabriele Wolf, Nicole Aumann, Marta Michalska, Antje Bast, Jürgen Sonnemann, James F Beck, Uwe Lendeckel, Philip Newsholme, and Reinhard Walther

Introduction Autoimmune destruction of pancreatic β cells during the development of type 1 diabetes is a complex process involving both cellular and humoral elements of cytotoxicity ( Mandrup-Poulsen et al . 1990 ). It is characterized by insulitis