نتایج جستجو برای: insulitis

تعداد نتایج: 749  

Journal: :Journal of immunology 2011
Jonathan Chee Eveline Angstetra Lina Mariana Kate L Graham Emma M Carrington Horst Bluethmann Pere Santamaria Janette Allison Thomas W H Kay Balasubramanian Krishnamurthy Helen E Thomas

TNF has been implicated in the pathogenesis of type 1 diabetes. When administered early in life, TNF accelerates and increases diabetes in NOD mice. However, when administered late, TNF decreases diabetes incidence and delays onset. TNFR1-deficient NOD mice were fully protected from diabetes and only showed mild peri-insulitis. To further dissect how TNFR1 deficiency affects type 1 diabetes, th...

Journal: :Proceedings of the National Academy of Sciences of the United States of America 2017
Michael Silverman Lindsay Kua Alessandro Tanca Mauro Pala Antonio Palomba Ceylan Tanes Kyle Bittinger Sergio Uzzau Christophe Benoist Diane Mathis

Certain MHC-II or HLA-D alleles dominantly protect from particular autoimmune diseases. For example, expression of the MHC-II Eα:Eβ complex potently protects nonobese diabetic (NOD) mice, which normally lack this isotype, from spontaneous development of type 1 diabetes. However, the underlying mechanisms remain debated. We investigated MHC-II-mediated protection from type 1 diabetes using a pre...

Journal: :Diabetes 2008
Conny Gysemans Evelyne van Etten Lutgart Overbergh Annapaula Giulietti Guy Eelen Mark Waer Annemieke Verstuyf Roger Bouillon Chantal Mathieu

OBJECTIVE Vitamin D deficiency increases risk for type 1 diabetes in genetically predisposed individuals, while high doses of 1,25-dihydroxyvitamin D(3) [1,25(OH)(2)D(3)] prevent insulitis and diabetes in NOD mice. RESEARCH DESIGN AND METHODS Since 1,25(OH)(2)D(3) regulates gene transcription through the vitamin D receptor (VDR), we investigated the role of VDR in diabetes development by crea...

Journal: :Diabetes 2004
Sarah E Eckenrode Qingguo Ruan Ping Yang Weipeng Zheng Richard A McIndoe Jin-Xiong She

cDNA microarrays with >11,000 cDNA clones from an NOD spleen cDNA library were used to identify temporal gene expression changes in NOD mice (1-10 weeks), which spontaneously develop type 1 diabetes, and changes between NOD and NOD congenic mice (NOD.Idd3/Idd10 and NOD.B10Sn-H2(b)), which have near zero incidence of insulitis and diabetes. The expression profiles identified two distinct groups ...

Journal: :Proceedings of the National Academy of Sciences of the United States of America 2000
D L Radu N Noben-Trauth J Hu-Li W E Paul C A Bona

Autoimmune insulin-dependent diabetes mellitus (IDDM) occurs spontaneously in mice-bearing transgenes encoding the influenza hemagglutinin under the control of the rat insulin promoter and a T cell receptor specific for an hemagglutinin peptide associated with I-E(d). Such "double transgenic" mice expressing wild-type or targeted IL-4Ralpha genes were examined for the onset of IDDM. Eight of 11...

Journal: :Proceedings of the National Academy of Sciences of the United States of America 1985
S Ikehara H Ohtsuki R A Good H Asamoto T Nakamura K Sekita E Muso Y Tochino T Ida H Kuzuya

An animal model [the nonobese diabetic (NOD) mouse] for type I diabetes features a striking infiltration of T cells into the pancreatic islets. This infiltration selectively destroys beta cells. Most of the T cells are Lyt-1+, but some are Lyt-2+,3+. Transfer experiments using parabiosis revealed that insulitis can be transferred within 2 weeks after parabiosis to immunoincompetent thymectomize...

2012
Takumi Tsuji Yuya Yoshida Tetsuro Fujita Takeyuki Kohno

UNLABELLED Aims/Introduction:  The therapeutic effectiveness against type 1 diabetes mellitus of a novel immunomodulator, FTY720 (fingolimod), in combination with sitagliptin, a dipeptidyl peptidase-4 inhibitor, was examined in the non-obese diabetic (NOD) mouse model. MATERIALS AND METHODS   Female NOD mice that had developed type 1 diabetes mellitus spontaneously were divided into four grou...

Journal: :Journal of autoimmunity 1999
I Krause Y Tomer D Elias M Blank B Gilburd I R Cohen Y Shoenfeld

The present study was undertaken to investigate whether active induction of systemic lupus erythematosus (SLE) in non-obese diabetic (NOD) mice could affect their development of insulin-dependent diabetes mellitus (IDDM). NOD mice were immunized with a human IgM mAb carrying the 16/6 idiotype (MIV-7) or with control human IgM. The mice were bled monthly and tested for SLE-associated autoantibod...

Journal: :Journal of immunology 2001
V Judkowski C Pinilla K Schroder L Tucker N Sarvetnick D B Wilson

Nonobese diabetic (NOD) mice spontaneously develop insulitis and destruction of pancreatic islet beta cells similar to type 1 diabetes mellitis in humans. Insulitis also occurs in the BDC2.5 TCR transgenic line of NOD mice that express the rearranged TCR alpha- and beta-chain genes of a diabetogenic NOD CD4 T cell clone. When activated with syngeneic islet cells in culture, BDC2.5 T cells adopt...

Journal: :Diabetes 2006
Jean M Jasinski Liping Yu Maki Nakayama Marcella M Li Myra A Lipes George S Eisenbarth Edwin Liu

A series of recent studies in humans and the NOD mouse model have highlighted the central role that autoimmunity directed against insulin, in particular the insulin B chain 9-23 peptide, may play in the pathogenesis of type 1 diabetes. Both pathogenic and protective T-cell clones recognizing the B:9-23 peptide have been produced. This report describes the successful creation of BDC12-4.1 T-cell...

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