scholarly journals Inhibition of Autoimmune Diabetes in Nonobese Diabetic Mice by Transgenic Restoration of H2-E MHC Class II Expression: Additive, But Unequal, Involvement of Multiple APC Subtypes

2001 ◽  
Vol 167 (4) ◽  
pp. 2404-2410 ◽  
Author(s):  
Ellis A. Johnson ◽  
Pablo Silveira ◽  
Harold D. Chapman ◽  
Edward H. Leiter ◽  
David V. Serreze
2013 ◽  
Vol 190 (12) ◽  
pp. 5961-5971 ◽  
Author(s):  
Alessandra De Riva ◽  
Mark C. Varley ◽  
Leslie J. Bluck ◽  
Anne Cooke ◽  
Michael J. Deery ◽  
...  

2000 ◽  
Vol 164 (12) ◽  
pp. 6610-6620 ◽  
Author(s):  
Pratibha Chaturvedi ◽  
Babita Agrawal ◽  
Marc Zechel ◽  
Edwin Lee-Chan ◽  
Bhagirath Singh

Author(s):  
Anne Cooke ◽  
Lorraine A. O'Reilly ◽  
Alan G. Baxter ◽  
Patricia Ozegbe ◽  
Patricia R. Hutchings ◽  
...  

2009 ◽  
Vol 88 (2) ◽  
pp. 160-169 ◽  
Author(s):  
Hong Cui ◽  
Carol Tucker-Burden ◽  
Sean M. D. Cauffiel ◽  
Adrienne K. Barry ◽  
Neal N. Iwakoshi ◽  
...  

2005 ◽  
Vol 79 (1) ◽  
pp. 619-621 ◽  
Author(s):  
Melissa A. Pierce ◽  
Anton Svetlanov ◽  
Marshall S. Horwitz ◽  
David V. Serreze

ABSTRACT The incidence of type 1 diabetes (T1D) is decreased in nonobese diabetic mice expressing the complete cassette of adenovirus early region 3 (E3) immunomodulating genes in pancreatic β cells. Embedded among the antiapoptotic E3 genes is one encoding an adenovirus death protein (ADP), which contributes to release of virion particles by promoting cell lysis. Because removal of this proapoptotic protein might have further enhanced the ability of E3 proteins to prevent T1D, an ADP-inactivated E3 construct was tested. Significantly, deletion of ADP did not improve the diabetes-protective effect of an E3 gene cassette.


2004 ◽  
Vol 199 (8) ◽  
pp. 1143-1151 ◽  
Author(s):  
Hsiang-Hsuan Sung ◽  
Jyuhn-Huarng Juang ◽  
Yu-Chun Lin ◽  
Chien-Hung Kuo ◽  
Jung-Tung Hung ◽  
...  

Decoy receptor 3 (DCR3) halts both Fas ligand– and LIGHT-induced cell deaths, which are required for pancreatic β cell damage in autoimmune diabetes. To directly investigate the therapeutic potential of DCR3 in preventing this disease, we generated transgenic nonobese diabetic mice, which overexpressed DCR3 in β cells. Transgenic DCR3 protected mice from autoimmune and cyclophosphamide-induced diabetes in a dose-dependent manner and significantly reduced the severity of insulitis. Local expression of the transgene did not alter the diabetogenic properties of systemic lymphocytes or the development of T helper 1 or T regulatory cells. The transgenic islets had a higher transplantation success rate and survived for longer than wild-type islets. We have demonstrated for the first time that the immune-evasion function of DCR3 inhibits autoimmunity and that genetic manipulation of grafts may improve the success and survival of islet transplants.


1993 ◽  
Vol 4 (4) ◽  
pp. 404-409 ◽  
Author(s):  
S. Ghosh ◽  
S.M. Palmer ◽  
N.R. Rodrigues ◽  
H.J. Cordell ◽  
C.M. Hearne ◽  
...  

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