|
Diabetes
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Expression of diabetes-resistant MHC class II I-Abeta chain molecules in NOD mice following retroviral transduction of autologous bone marrow hematopoietic stem cells prevented the development of autoreactive T cells by intrathymic deletion and protected the mice from the development of insulitis and diabetes.
|
15467836 |
2004 |
|
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 |
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 |
Three of these four genes colocalize with NOD mouse diabetes susceptibility genes--the strongest concordance identified to date between any two autoimmune diseases--reflecting the association between autoimmune diabetes and type 1 gastritis in humans.
|
15763989 |
2005 |
|
Diabetes
|
0.100 |
Biomarker
|
disease |
BEFREE |
Using an F2(B6 x NOD) cross in a genome-wide scan, we map the control of this trait to a region on chromosome 4 (logarithm of odds score, 4.4) which includes the Idd11 and Idd9 diabetes susceptibility loci, supporting the hypothesis that this B cell trait is related to the development of diabetes in the NOD mouse.
|
15814708 |
2005 |
|
Diabetes
|
0.100 |
Biomarker
|
disease |
BEFREE |
Although Idd21.1 did not influence beta-islet inflammation, splenocytes from pre-diabetic Idd21.1-congenic mice were less efficient at transferring diabetes to immunodeficient NOD-scid mice.
|
16123376 |
2005 |
|
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 |
A single administration of rAd-GLP-1 via the tail vein into streptozotocin (STZ)-induced diabetic non-obese diabetic/severe combined immunodeficient (NOD/SCID) mice resulted in remission of diabetes within 10 days; normoglycemia remained until the experiment was terminated.
|
17164779 |
2007 |
|
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 |
Biomarker
|
disease |
BEFREE |
Remarkably, as few as 1,000 BDC-10.1 Rg T-cells caused rapid diabetes following adoptive transfer into NOD.scid mice.
|
18299317 |
2008 |
|
Diabetes
|
0.100 |
Biomarker
|
disease |
BEFREE |
A plasmid DNA vaccine encoding mouse proinsulin II reduced the incidence of diabetes in a mouse model of type I diabetes when administered to hyperglycemic (therapeutic mode) or normoglycemic (prophylactic mode) NOD mice.
|
19050246 |
2008 |
|
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 |
Biomarker
|
disease |
BEFREE |
NOD/SCID mice in which diabetes was induced by streptozotocin injection were transplanted with human pancreatic islet cells.
|
18420485 |
2008 |
|
Diabetes
|
0.100 |
Biomarker
|
disease |
BEFREE |
In both the NOD mouse and diabetes-prone BB (BBDP) rat, TLR upregulation can suppress disease.
|
19199942 |
2009 |
|
Diabetes
|
0.100 |
Biomarker
|
disease |
BEFREE |
Our data identify miR-21, miR-34a, and miR-146a as novel players in beta-cell failure elicited in vitro and in vivo by proinflammatory cytokines, notably during the development of peri-insulitis that precedes overt diabetes in NOD mice.
|
20086228 |
2010 |
|
Diabetes
|
0.100 |
Biomarker
|
disease |
BEFREE |
By using the recombinant PLAD.Fc protein to block TNFR1 assembly, we demonstrated that PLAD.Fc treatment significantly reduced the TNFR1-driving proinflammatory cytokines and protected NOD mice from diabetes.
|
21689905 |
2011 |
|
Diabetes
|
0.100 |
Biomarker
|
disease |
BEFREE |
Intramuscular vaccination of recombinant adeno-associated virus to 10-wk-old NOD female mice and a subsequent 3 wk induction of IL-2 was sufficient to prevent diabetes and block the progression of insulitis.
|
21317396 |
2011 |
|
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 |
Biomarker
|
disease |
BEFREE |
Differential IL-21 signaling in APCs leads to disparate Th17 differentiation in diabetes-susceptible NOD and diabetes-resistant NOD.Idd3 mice.
|
22019586 |
2011 |
|
Diabetes
|
0.100 |
Biomarker
|
disease |
BEFREE |
IL-7 uniquely maintains FoxP3(+) adaptive Treg cells that reverse diabetes in NOD mice via integrin-β7-dependent localization.
|
21745722 |
2011 |
|
Diabetes
|
0.100 |
Biomarker
|
disease |
BEFREE |
Transplantation of human islets reconstituted with Adv-hHGF-hIL-1Ra transduced hBMSCs under the kidney capsule of streptozotocin-induced diabetic non-obese diabetic/severe combined immunodeficient (NOD-SCID) mice reversed diabetes by reducing blood glucose levels to ≤ 200 mg/dL for up to 15 weeks and reduced the number of islets required to achieving normoglycemia.
|
21499838 |
2011 |
|
Diabetes
|
0.100 |
Biomarker
|
disease |
BEFREE |
Glyphosine, a pocket 9 compound, enhances insulin peptide presentation to T cells at concentrations as low as 10 nM, upregulates IL-10 secretion, and prevents diabetes in NOD mice.
|
22043012 |
2011 |
|
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 |
Biomarker
|
disease |
BEFREE |
We show that combination therapy with low-dose systemic anti-CD3 stably reverted diabetes in NOD mice and increased frequencies of local Tregs, which not only accumulated in the pancreatic islets, but also suppressed immune response in an autoantigen-specific way.
|
22484814 |
2012 |
|
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 |