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.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117 Front+Endocrinol+(Lausanne)
2018 ; 9
(ä): 51
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The Role of NOD Mice in Type 1 Diabetes Research: Lessons from the Past and
Recommendations for the Future
#MMPMID29527189
Chen YG
; Mathews CE
; Driver JP
Front Endocrinol (Lausanne)
2018[]; 9
(ä): 51
PMID29527189
show ga
For more than 35?years, the NOD mouse has been the primary animal model for
studying autoimmune diabetes. During this time, striking similarities to the
human disease have been uncovered. In both species, unusual polymorphisms in a
major histocompatibility complex (MHC) class II molecule confer the most disease
risk, disease is caused by perturbations by the same genes or different genes in
the same biological pathways and that diabetes onset is preceded by the presence
of circulating autoreactive T cells and autoantibodies that recognize many of the
same islet antigens. However, the relevance of the NOD model is frequently
challenged due to past failures translating therapies from NOD mice to humans and
because the appearance of insulitis in mice and some patients is different.
Nevertheless, the NOD mouse remains a pillar of autoimmune diabetes research for
its usefulness as a preclinical model and because it provides access to invasive
procedures as well as tissues that are rarely procured from patients or controls.
The current article is focused on approaches to improve the NOD mouse by
addressing reasons why immune therapies have failed to translate from mice to
humans. We also propose new strategies for mixing and editing the NOD genome to
improve the model in ways that will better advance our understanding of human
diabetes. As proof of concept, we report that diabetes is completely suppressed
in a knock-in NOD strain with a serine to aspartic acid substitution at position
57 in the MHC class II A?. This supports that similar non-aspartic acid
substitutions at residue 57 of variants of the human class II HLA-DQ? homolog
confer diabetes risk.
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