|
Diabetes
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Prevention of diabetes in the NOD mouse by a Th1 clone specific for a hsp60 peptide.
|
10677244 |
2000 |
|
Diabetes
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
NOD Idd5 locus controls insulitis and diabetes and overlaps the orthologous CTLA4/IDDM12 and NRAMP1 loci in humans.
|
11016460 |
2000 |
|
Diabetes
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
It can be induced by as disparate means as tuberculin antigen administration, by interleukin-4 treatments, by transfer of T-cell lines generated in autologous mixed lymphocyte responses, and by immunization to insulin B-chain, whereas oral islet cell antigens, such as insulin, can delay diabetes onset in the NOD mouse.(ABSTRACT TRUNCATED AT 250 WORDS)
|
8100786 |
1993 |
|
Diabetes
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
G6pc2(-/-) mice were generated on the NOD/ShiLtJ genetic background, and glycemia was monitored weekly up to 35 weeks of age to determine the onset and incidence of diabetes.
|
21896930 |
2011 |
|
Diabetes
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
While both isoforms of glutamic acid decarboxylase (GAD) function as important autoantigens in autoimmune diabetes mellitus-GAD65 in humans and GAD67 in the NOD mouse-GAD67 is not synthesized in human pancreatic islets and is thought not to be an autoantigen in human diabetes.
|
12515288 |
2002 |
|
Diabetes
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
We demonstrated that givinostat synergised with otelixizumab to induce durable remission of diabetes in 80% of recently diabetic NOD-huCD3ε mice.
|
29030662 |
2018 |
|
Diabetes
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Because type 1 diabetes is regarded to be immune-mediated and vitamin D prevents the development of diabetes in the NOD mouse, we investigated the role of the vitamin D receptor (VDR) gene as a candidate for type 1 diabetes susceptibility.
|
10868975 |
2000 |
|
Diabetes
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
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 Aβ.
|
29527189 |
2018 |
|
Diabetes
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
First, to see which immunomodulating molecule-secreting islet grafts can most powerfully prevent diabetes development in NOD mice without immunosuppressant, NOD islets were transfected with one of the following adenoviral vectors: Ad.IL-12p40, Ad.TGF-beta, Ad.CTLA4-Ig, or Ad.TNF-alpha after which they were transplanted under the renal capsule of acutely diabetic NOD mice.
|
18400329 |
2008 |
|
Diabetes
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Subsequent analyses found syngeneic splenocytes bearing the combination of the two ECDI-coupled IGRPs but not INS peptides (IGRP-SPs or INS-SPs) effectively inhibited diabetes development in NOD.β2m(null).HHD mice.
|
21346176 |
2011 |
|
Diabetes
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Furthermore, the transduced cells could be used for studies in the NOD mouse system without altering the onset of diabetes.
|
15144890 |
2004 |
|
Diabetes
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
NOR mice are insulitis resistant and diabetes free despite genetic identity with NOD at numerous chromosomal regions containing previously described insulin-dependent diabetes (Idd) genes, including the strongly diabetogenic H2g7 major histocompatibility complex (MHC) haplotype.
|
7931087 |
1994 |
|
Diabetes
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Thus, CD11c(+)CD11b(+) DC and pDC have countervailing actions in NOD diabetes, with myeloid DC providing critical antigenic stimulation to naive CD4(+) T cells and pDC providing regulatory control of CD4(+) T cell function in the target tissue.
|
17911589 |
2007 |
|
Diabetes
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
The severity of insulitis in NOD.PD-L1Tg mice was significantly lower than in NOD mice and none developed diabetes.
|
31419705 |
2019 |
|
Diabetes
|
0.100 |
Biomarker
|
disease |
BEFREE |
P2X7R blockade with oxidized ATP reduces the CD8<sup>+</sup> T cell-mediated autoimmune response in vitro and delays diabetes onset in NOD mice.
|
30065030 |
2018 |
|
Diabetes
|
0.100 |
Biomarker
|
disease |
BEFREE |
We conclude that IA-2beta is involved in insulin secretion, but despite its importance as a major autoantigen in human type 1 diabetes, it is not required for the development of diabetes in NOD mice.
|
15220191 |
2004 |
|
Diabetes
|
0.100 |
Biomarker
|
disease |
BEFREE |
Fenofibrate, a regulator of sphingolipid metabolism, is known to prevent diabetes in NOD mice.
|
31410530 |
2019 |
|
Diabetes
|
0.100 |
Biomarker
|
disease |
BEFREE |
We found that the CD19+IgM+ cell is the primary subpopulation of B cells that delayed transfer of diabetes mediated by diabetogenic T cells from NOD mice (P = 0.002).
|
30518692 |
2018 |
|
Diabetes
|
0.100 |
Biomarker
|
disease |
BEFREE |
In the resulting 3A9 TCR:iHEL NOD.H2(k)-Chr12 mice, we observed a significant decrease in diabetes incidence as well as a decrease in both the quantity and affinity of HEL-specific IgG autoantibodies relative to 3A9 TCR:iHEL NOD.H2(k) mice.
|
25623266 |
2015 |
|
Diabetes
|
0.100 |
Biomarker
|
disease |
BEFREE |
Available experiments in the NOD mouse and epidemiological evidence in the human point to proinsulin as a key autoantigen in diabetes.
|
16306346 |
2005 |
|
Diabetes
|
0.100 |
Biomarker
|
disease |
BEFREE |
Despite the well known role of nucleotide oligomerization domain (NOD) receptor proteins in innate immunity, their association with diabetes is less explored.
|
24018334 |
2013 |
|
Diabetes
|
0.100 |
Biomarker
|
disease |
BEFREE |
Islets were isolated from NOD mice and mice treated with multiple low doses of streptozotocin, as a mouse model of diabetes.
|
28280903 |
2017 |
|
Diabetes
|
0.100 |
Biomarker
|
disease |
BEFREE |
Furthermore, splenocytes from NOD-Alox15(null) mice are unable to transfer diabetes in an adoptive transfer model.
|
23437231 |
2013 |
|
Diabetes
|
0.100 |
Biomarker
|
disease |
BEFREE |
This was demonstrated by greater ability to cause recurrent diabetes in NOD-RIP-CD86 diabetic mice transplanted with 6-wk-old NOD islets and adoptively transferred diabetes from diabetic NOD-RIP-CD86 mice to NOD.scid mice.
|
17947667 |
2007 |
|
Diabetes
|
0.100 |
Biomarker
|
disease |
BEFREE |
Because exogenous IL-4 and IL-10 exert antidiabetogenic effect in NOD mice and early blockade of endogenous tumor necrosis factor-alpha prevents NOD mouse diabetes, these phenomena may be causally related to the antidiabetogenic effect of HGG-pulsed DC treatment.
|
10746656 |
2000 |