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1 corticosterone were investigated using male nonobese diabetic mice.
2 ferred 5 x 10(6) splenocytes from 6-week-old nonobese diabetic mice.
3 oimmune diabetes developing spontaneously in nonobese diabetic mice.
4 otocin and during development of diabetes in nonobese diabetic mice.
5 tolerance and the development of diabetes in nonobese diabetic mice.
6 ng grafted and endogenous islets in diabetic nonobese diabetic mice.
7 antigen-specific Tregs from autoimmune-prone nonobese diabetic mice.
8 the onset and severity of type 1 diabetes in nonobese diabetic mice.
9 independent in T cells from autoimmune-prone nonobese diabetic mice.
10 a small population of Ag-specific T cells in nonobese diabetic mice.
11 uction protocol is ineffective in autoimmune nonobese diabetic mice.
12 nize these peptides in type 1 diabetes-prone nonobese diabetic mice.
13 ion protein (LTbetaR-Ig) was administered to nonobese diabetic mice.
14 level of EF-1alpha mRNA was also observed in nonobese diabetic mice.
15 II molecule DQ in humans and to MHC I-Ag7 in nonobese diabetic mice.
16 e sclerosis, and prevents type 1 diabetes in nonobese diabetic mice.
17 tes mellitus by the CD4+ Th1 clone BDC2.5 to nonobese diabetic mice.
18 cell-specific injury or from the pancreas of nonobese diabetic mice.
19 duced a long-term diabetes-free condition in nonobese diabetic mice.
23 vation and whose adoptive transfer protected nonobese diabetic mice against type 1 diabetes (T1D).
26 on-associated lymphoid neogenesis, including nonobese diabetic mice, also exhibit concomitant express
27 experimental autoimmune encephalomyelitis in nonobese diabetic mice, an experimental model that resem
29 cific MHC class II genes, such as I-A(g7) in nonobese diabetic mice and HLA-DQ8 in humans, suggests t
30 work from one laboratory has shown, in both nonobese diabetic mice and humans, an association betwee
31 oth muscle, and neurons were investigated in nonobese diabetic mice and organotypic cultures by immun
32 m-3 pathway blockade accelerated diabetes in nonobese diabetic mice and prevented acquisition of tran
33 completely prevented diabetes development in nonobese diabetic mice and strongly reduced its incidenc
36 chanisms underlying this observation, female nonobese diabetic mice at 4, 8, and 12 wk of age were gi
37 amounts of insulin (ins) to cure diabetes in nonobese diabetic mice but, unlike transplanted islets,
38 reverses established autoimmune diabetes in nonobese diabetic mice by restoring self-tolerance, and
41 ogenesis of diabetes, we generated NOD mice (nonobese diabetic mice developing spontaneous autoimmune
43 nce of type 1 diabetes (T1D) is decreased in nonobese diabetic mice expressing the complete cassette
46 Fas (lpr) or FasL (gld) completely protects nonobese diabetic mice from autoimmune diabetes but also
51 MM model in severe combined immunodeficient/nonobese diabetic mice in which diffuse MM lesions devel
52 n B13 autoantibodies in young diabetes-prone nonobese diabetic mice is associated with reduced inflam
53 ze that resistance to tolerance induction in nonobese diabetic mice is due to the presence of memory
54 ent population of pathogenic CD8+ T cells in nonobese diabetic mice is islet-specific glucose-6-phosp
55 n a model of passive transfer of diabetes in nonobese diabetic mice, lytic IL-2/Fc, but not nonlytic
56 ia was created by femoral artery ligation in nonobese diabetic mice (NOD mice, n = 20) and in control
61 sion of tumor necrosis factor (TNF)-alpha in nonobese diabetic mice promotes diabetes by provoking is
62 tes-inducing CD4 T cell clones isolated from nonobese diabetic mice recognize epitopes formed by cova
63 ocking the SDF-1alpha/CXCR4 axis in IFNgamma-nonobese diabetic mice resulted in diminished proliferat
64 d leukemic cell lines into immunocompromised nonobese diabetic mice resulted in significant elevation
65 enic intermediate lobe tissues into diabetic nonobese diabetic mice resulted in the restoration of ne
69 e 1 or type 2 diabetes, and in the islets of nonobese diabetic mice that have developed insulitis or
70 pe recognized by pathogenic T lymphocytes in nonobese diabetic mice, the animal model for type 1 diab
71 sed Fah(-/-), Rag2(-/-), Il2r(-/-) mice with nonobese diabetic mice to create FRGN mice, whose livers
72 (Treg cells) during diabetes progression in nonobese diabetic mice was investigated to determine whe
76 ccelerated BDC2.5 T-cell receptor transgenic nonobese diabetic mice, which experience development of
78 xpression of NMI was detected in islets from nonobese diabetic mice with insulitis and in rodent or h
80 oliferation using in vivo teratoma assays in nonobese diabetic mice with severe combined immunodefici
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