ライフサイエンスコーパス: NOD mice

1 promising approach for diabetes reversal in NOD mice.

2 enotype and delayed the onset of diabetes in NOD mice.

3 and in preventing and reversing diabetes in NOD mice.

4 , but not Srsf10, in the PLNs of NOD.B10 and NOD mice.

5 n the pancreas and pancreatic lymph nodes of NOD mice.

6 interferon regulatory factor 5 compared with NOD mice.

7 vo after anti-CD3 administration in diabetic NOD mice.

8 ed against spontaneous development of T1D in NOD mice.

9 equently an enduring reversal of diabetes in NOD mice.

10 cited tolerogenic CD4(+) T-cell responses in NOD mice.

11 s and beta-cell fitness and viability in the NOD mice.

12 pancreatic beta cells compared with control NOD mice.

13 red autoimmune response and T1D incidence in NOD mice.

14 nd may function as the autoimmune trigger in NOD mice.

15 7 cells for stability and diabetogenicity in NOD mice.

16 vely restore normoglycemia in newly diabetic NOD mice.

17 and this role is disrupted in diabetes-prone NOD mice.

18 ot prevent diabetes onset in immunocompetent NOD mice.

19 he initiation and progression of diabetes in NOD mice.

20 n in peritoneal macrophages from C57BL/6 and NOD mice.

21 M-1 blockade triggers neuritis only in young NOD mice.

22 nsistent feature of the islet infiltrates of NOD mice.

23 5 weeks of age]) safely prevents diabetes in NOD mice.

24 of thymic involution that is accelerated in NOD mice.

25 diabetes development in both male and female NOD mice.

26 to promote progression to overt diabetes in NOD mice.

27 suppressed development of type-1 diabetes in NOD mice.

28 eactive B and T cells endogenously primed in NOD mice.

29 out affecting beta-cell proliferation in the NOD mice.

30 rs homing to the liver and pancreas of adult NOD mice.

31 /alum, with GABA treatment in newly diabetic NOD mice.

32 ele is required for type 1 diabetes (T1D) in NOD mice.

33 rom young, but not older, prediabetic female NOD mice.

34 ) mice and by the use of a TLR9 inhibitor in NOD mice.

35 ppressed late preclinical type 1 diabetes in NOD mice.

36 to localize IL-2 expression to the islets of NOD mice.

37 broad autoimmune response by CD4 T cells in NOD mice.

38 r antidiabetogenic properties than wild-type NOD mice.

39 t hours and days after anti-CD3 treatment of NOD mice.

40 d IFN-gamma, and infiltrated the pancreas in NOD mice.

41 autoimmune B6 mice but not in diabetes-prone NOD mice.

42 nctual perturbation of T reg cells in BDC2.5/NOD mice.

43 Pro motif enhance self-reactivity in VH125Tg/NOD mice.

44 in the pancreas of prediabetic and diabetic NOD mice.

45 o) subsets, infiltrate islets of prediabetic NOD mice.

46 D40:Fc) was injected locally into the SGs of NOD mice.

47 al checkpoint breakthrough in Rag1-deficient NOD mice.

48 ory genes and protection against diabetes in NOD mice.

49 on in Th1 cells, similar to that observed in NOD mice.

50 m peripheral lymphoid tissues in TLR9(-)/(-) NOD mice.

51 sed in macrophages, but not B and T cells of NOD mice.

52 production in CD4(+) T cells in TLR9(-)/(-) NOD mice.

53 fficient (WB/B6), MC-deficient (W/W(v)), and NOD mice.

54 was slightly increased in nondiabetic adult NOD mice.

55 in alloxan-induced diabetic and spontaneous NOD mice.

56 ith colonic microbiota-responsive T cells in NOD mice.

57 h rapamycin (RAPA) prevents hyperglycemia in NOD mice.

58 pathway genes are found in the hyperglycemic NOD mice.

59 development in prediabetic hCD20 transgenic NOD mice.

60 and diabetes was reversed in newly diagnosed NOD mice.

61 teraction significantly delayed T1D onset in NOD mice.

62 e human population, a potential benefit over NOD mice.

63 d also strongly inhibited T1D development in NOD mice.

64 atment duration for the prevention of T1D in NOD mice.

65 t were also expanded within the pancreata of NOD mice.

66 on and development of autoimmune diabetes in NOD mice.

67 absolute number between the C57BL/6 and the NOD mice.

68 ion of CD4(+) T cells residing in the PLN of NOD mice.

69 eptor therapy reverses diabetes in new onset NOD mice.

70 pressed type 1 diabetes (T1D) progression in NOD mice.

71 pression is reduced in Valpha14iNKT cells of NOD mice.

72 RISPR-Cas9 for direct genetic alternation of NOD mice.

73 ated diabetes development in c-Rel-deficient NOD mice.

74 ing early-onset autoimmune diabetogenesis in NOD mice.

75 e pancreatic lymph nodes (PLN) and islets of NOD mice.

76 -1) blockade to reverse new-onset disease in NOD mice.

77 iled to develop in Btk-deficient Notch2(+/-)/NOD mice.

78 T-cell infiltration in pancreatic islets in NOD mice.

79 ndividual islets of spontaneously autoimmune NOD mice.

80 PD-L1-driven tolerance, reverses diabetes in NOD mice.

81 slets from diabetes-prone nonobese diabetic (NOD) mice.

82 vely, in autoimmune-prone nonobese diabetic (NOD) mice.

83 g from healthy (C57BL/6) and diabetes-prone (NOD) mice.

84 type 1 diabetes (T1D) in nonobese diabetic (NOD) mice.

85 1 diabetes in humans and non-obese diabetic (NOD) mice.

86 lated NOD.IFN-gamma(null) , but not standard NOD, mice.

87 atory immune system that was also evident in NOD mice, a model of type 1 diabetes, born by C-section.

88 NOD mice, a model strain for human type 1 diabetes, expr

89 ased tear secretion from non-obese diabetic (NOD) mice, a model of autoimmune dacryoadenitis, when ad

90 e autoimmune responses in nonobese diabetic (NOD) mice, a spontaneous disease model for type 1 diabet

91 mmation accompanies type 1 diabetes (T1D) in NOD mice, affecting organs like thyroid and salivary gla

92 s significantly higher than that of diabetic NOD mice after the injection of MN-Ex10-Cy5.5, indicatin

93 L22 in Treg recruitment in the protection of NOD mice against type 1 diabetes following the treatment

94 y accelerated insulitis and hyperglycemia in NOD mice along with a substantial reduction in T-regulat

95 In NOD mice and also likely humans, B lymphocytes play an i

96 lopment is ultimately mediated by T-cells in NOD mice and also likely humans, B-lymphocytes play an a

97 NOD mice and BALB/c controls were labeled continuously w

98 We investigated pain mechanisms in NOD mice and compared it to C57BL/6 (B6) mice, a strain

99 ntigen IGRP (NRP-V7-reactive) in prediabetic NOD mice and compared them to others that shared their p

100 olated cells from the islet of Langerhans of NOD mice and cultured them in vitro.

101 To track IAPP-reactive T cells in NOD mice and determine how they contribute to the pathog

102 chyma to the sinusoids in the bone marrow of NOD mice and enter the periphery unimpeded.

103 APCs, is shared between diabetes-susceptible NOD mice and human T1D patients.

104 sociation with a macrophage subpopulation in NOD mice and human type 1 diabetic samples and, hence, p

105 o follow autoimmune pathogenesis, similar to NOD mice and humans, characterized by hyperglycemia requ

106 x (IM), in development of type 1 diabetes in NOD mice and in human type 1 diabetes.

107 n correlates with the severity of disease in NOD mice and is reduced in the PLNs of mice that do not

108 he primary source of anti-insulin B cells in NOD mice and suggest that dysregulation of central toler

109 We expressed an I-Ealpha(kloxP) transgene in NOD mice and used cell type-specific I-E ablation to sho

110 ated from islets of young nonobese diabetic (NOD) mice and nondiabetic mice as well as from nondiabet

111 s, and that hyperglycemic nonobese diabetic (NOD) mice and T1D patients lack these potent negative re

112 ession promoted islet vascular remodeling in NOD mice, and inhibition of VEGFR activity with RTKIs ab

113 ptor (Th40 cells) are highly diabetogenic in NOD mice, and NOD.BDC2.5.TCR.Tg mice possess large numbe

114 CD40:Fc was stably expressed in the SG of NOD mice, and the protein was secreted into the blood st

115 As disease unfolded in NOD mice, anti-PRPH B cells invaded the islets and incre

116 hat both incidence and progression of T1D in NOD mice are independent of mast cells.

117 I-A(g7), the unique MHC class II molecule of NOD mice, are presented in islets and in pancreatic lymp

118 ificantly reduce diabetes incidence in 125Tg/NOD mice as it does in NOD mice with a normal B cell rep

119 infiltration and activation in pancreata of NOD mice as well as humanized NOD Scid IL2 receptor gamm

120 (I-A(b-g7)) in wild-type nonobese diabetic (NOD) mice, as well as NOD mice coexpressing a diabetogen

121 ng most Gram-negative bacteria in the gut of NOD mice at different time points in their life, using a

122 on of insulin-binding B cells is apparent in NOD mice at the earliest point of Ag commitment in the b

123 Injection of NOD mice at the prediabetic age and early hyperglycemic

124 ), is gradually diminished in alpha-cells of NOD mice, autoantibody-positive (AA(+)) and overtly type

125 A subpopulation of diabetic NOD mice became hypothermic, and tau hyperphosphorylatio

126 or, for 2 weeks to female nonobese diabetic (NOD) mice, beginning at 3 weeks of age, followed by twic

127 subcutaneously in autoimmune diabetes-prone NOD mice, beta-cell-reactive T cells homed to these scaf

128 nce of lymph node stromal cells (LNSCs) from NOD mice but not from mice lacking the PI epitope.

129 k of TSSP expression conferred protection in NOD mice but not in C57BL/6 mice.

130 egative selection of autoreactive T cells in NOD mice, but it is still unclear how mixed chimerism to

131 ion, accelerated MHCII turnover may occur in NOD mice, but it reflects environmental and developmenta

132 Many autoreactive T cells are found in NOD mice, but not all have a major role in the initiatio

133 or proinsulin does not protect hyperglycemic NOD mice, but the combination with proinsulin offers lim

134 his autoimmune disease in nonobese diabetic (NOD) mice, but the environmental cues that govern macrop

135 improves beta cell function and survival in NOD mice by enhancing the unfolded protein response and

136 ction of neo-islets in the liver of diabetic NOD mice by gene transfer of Neurogenin3, the islet-defi

137 onset of spontaneous autoimmune diabetes in NOD mice by inhibiting insulitis and augmenting regulato

138 in T cells attenuates autoimmune diabetes in NOD mice by preferentially modulating TCR signaling-medi

139 congenic mouse strain was generated in which NOD mice carry the full Idd22 confidence interval.

140 d (unstable) forms of IGRP in IGRP-deficient NOD mice carrying MHC class I-deficient beta-cells, dend

141 In NOD mice, CD11c(+) cells increase greatly with islet inf

142 In late diabetic NOD mice, CD4 T cells were found as well as a weak antib

143 ype nonobese diabetic (NOD) mice, as well as NOD mice coexpressing a diabetogenic and I-A(g7)-restric

144 levated in the islets of non-obese diabetic (NOD) mice compared with controls.

145 ts of Langerhans in young nonobese diabetic (NOD) mice contained two antigen-presenting cell (APC) po

146 commenced in already insulin autoantibody(+) NOD mice, continuous BAFFR-Fc treatment alone or in comb

147 rom a transgene in K cells and nontransgenic NOD mice (controls); pancreas and duodenum tissues were

148 icate that excessive NKT17 cell frequency in NOD mice correlates with defective Th-POK expression by

149 In this study, we demonstrate that NOD mice deficient for isoforms of ICAM-1, which comedia

150 In this study, NOD mice deficient for the HR have been generated by mea

151 of reactive oxygen species (ROS) in T1D, as NOD mice deficient in NADPH oxidase (NOX)-derived supero

152 irectly test their involvement, we generated NOD mice deficient in type I IFN receptors (NOD.IFNAR1(-

153 ploying cell-sorted skin equivalents in SCID/NOD mice demonstrated enhanced transepidermal water loss

154 ither promote or suppress T1D development in NOD mice depending on where it is expressed.

155 In NOD mice depleted of islet-resident macrophages starting

156 s support T cell-mediated type 1 diabetes in NOD mice, despite being anergic to B cell mitogens and T

157 TLR9-deficient (TLR9(-)/(-)) NOD mice develop a significantly reduced incidence of di

158 After EAP induction, NOD mice developed a specific cellular response characte

159 er inducing IFN beta (TRIF) double deficient NOD mice developed the disease.

160 ult female NOD mice were examined, but young NOD mice did not display tau hyperphosphorylation.

161 In NOD mice, dietary intervention with omega-3 PUFAs sharpl

162 dly, the majority of Ag-experienced cells in NOD mice displayed an anergic phenotype, but this popula

163 , and restored normoglycemia in recent-onset NOD mice, even when hyperglycemia was severe at diagnosi

164 Icam1(tm1Jcgr)NOD mice exhibit a specifically altered TCR repertoire.

165 reveal that precursors of mature B cells in NOD mice exhibit an altered migration set point, allowin

166 Prediabetic NOD mice exhibit hyperglucagonemia, possibly due to an i

167 NOD mice exhibit major defects in the earliest stages of

168 These Icam1(tm1Jcgr)NOD mice exhibit unaltered numbers of regulatory T cells

169 Islet Foxp3(+)Tregs in dsAAVmIP-IL2-treated NOD mice exhibited enhanced fitness marked by increased

170 Cyclin D3-deficient NOD mice exhibited exacerbated diabetes and impaired glu

171 IGRP206-214-specific T cells in NOD mice expand, acquire the phenotype of effector-memor

172 CD4+ T cells in CP-1-infected NOD mice expressed IFN-gamma and IL-17A but not IL-4, co

173 experimental autoimmune thyroiditis (EAT) in NOD mice expressing human DRbeta1-Arg74.

174 ficiency did not suppress T1D development in NOD mice expressing the transgenic NY8.3 CD8 TCR.

175 ing T1D in MyD88-negative (but not wild-type NOD mice), favoring the balanced signal hypothesis.

176 Thymic epithelium from Icam1(tm1Jcgr)NOD mice features an altered expression of costimulatory

177 In specific pathogen-free nonobese diabetic (NOD) mice, females have 1.3-4.4 times higher incidence o

178 san, results in a superior protection of the NOD mice from diabetes as compared with mice that receiv

179 yxin B, and streptomycin treatment protected NOD mice from diabetes development through alterations i

180 Both I-A transgenes protected NOD and 4.1-NOD mice from diabetes.

181 Idd5 are able to partially protect congenic NOD mice from insulitis and diabetes, and to partially t

182 ell Ag resulted in an enhanced protection of NOD mice from T1D as compared with treatment with beta-g

183 CSF/CpG)/insulin-MP vaccine protected 40% of NOD mice from T1D.

184 icrobiome to confer protection to adult male NOD mice from type 1 diabetes.

185 d with the development of type 1 diabetes in NOD mice) from those selected by a non-autoimmunity-prom

186 Promisingly, NOD mice given transient late disease stage BAFFR-Fc mon

187 We found that NOD mice had approximately 50% less fat mass and were 2-

188 To determine whether autoimmune NOD mice have alterations in type 1 IFN innate responsiv

189 Finally, (pre)diabetic NOD mice have autoantibodies and effector T cells that r

190 Type 1 diabetic NOD mice have defects in both thymic negative selection

191 Studies in NOD mice have provided important insight into the geneti

192 We bred NOD mice hemizygous at both TCRalpha and beta (TCRalpha(

193 es susceptibility in T1D non-obese diabetic (NOD) mice, identifying immune-independent beta cell frag

194 1 hinders the development and onset of SS in NOD mice, in part by suppressing IFN-gamma production.

195 vage of vehicle (dH2O) in nonobese diabetic (NOD) mice induced a social avoidance behavior that was n

196 Of note, DeltaT2 of prediabetic and diabetic NOD mice injected with MN-Cy5.5 was not significantly ch

197 ined that increased MZ B cell development in NOD mice is independent of T cell autoimmunity, BCR spec

198 e 1 to double negative 2 stage thymocytes in NOD mice is inefficient; however, this defect is compens

199 The incidence of T1D in NOD mice is influenced by the degree of cleanliness of t

200 ural regulatory T cell (Treg) compartment of NOD mice is unusual in having reduced TCR diversity desp

201 pe 1 diabetes mellitus in nonobese diabetic (NOD) mice is insulin.

202 of recipient mice implanted with thymi from NOD mice lacking expression of the autoimmune regulator

203 d by the microbiota were revealed by testing NOD mice lacking MyD88 in combination with knockouts of

204 Surprisingly, the findings indicate that NOD mice lacking the HR (13R(-/-)) display resistance to

205 ur data indicate that insulin dysfunction in NOD mice leads to AD-like tau hyperphosphorylation in th

206 poxygenase enzyme (12/15-LO, Alox15 gene) in NOD mice leads to nearly 100 percent protection from T1D

207 The T cells persisted in hyperglycemic NOD mice maintained with an insulin pellet despite destr

208 n be transferred to naive nonobese diabetic (NOD) mice [model of type 1 diabetes (T1D)] by transfer o

209 on during T1D pathogenesis, as NOX-deficient NOD mice (NOD.Ncf1(m1J) ) were protected against T1D due

210 Despite widespread use of nonobese diabetic (NOD) mice, NOD with severe combined immunodeficiency (sc

211 ns of mast cell-deficient nonobese diabetic (NOD) mice, NOD.Cpa3(Cre/+) (Heidelberg) and NOD.Kit(W-sh

212 address this issue, we generated transgenic NOD mice (nonobese diabetic) in which Ptpn22 can be indu

213 test disease contributions of MZ B cells in NOD mice, Notch2 haploinsufficiency (Notch2(+/-)) was in

214 ut only in conditions in which the recipient NOD mice or NOD.Rag1(-/-) mice were subjected to light i

215 ells isolated from either nonobese diabetic (NOD) mice or humans with T1D.

216 ucose responsiveness; conversely, transgenic NOD mice overexpressing cyclin D3 in beta cells exhibite

217 cures recent-onset type 1 diabetes (T1D) in NOD mice, partially by boosting pancreatic regulatory T

218 In islets, expression of 12/15-LO in NOD mice peaks at a crucial time during insulitis develo

219 l to restore normoglycemia in newly diabetic NOD mice, perhaps because too few beta-cells remain by t

220 Anti-insulin B cells in 125Tg/Notch2(+/-)/NOD mice populate an enlarged MZ, suggesting that low-le

221 trating oral insulin does not prevent T1D in NOD mice, possibly due to antigen digestion prior to muc

222 In response to CpG, NOD mice produce more type 1 IFN and express higher leve

223 These data suggest that NOD mice promote tolerance through anergy induction, but

224 xpression of I-E on dendritic cells (DCs) of NOD mice promotes the differentiation of MHC promiscuous

225 Further, oral administration of AEA to NOD mice provides protection from T1D.

226 rapy for restoring normoglycemia in diabetic NOD mice, providing important preclinical evidence for t

227 Weaning NOD mice received low doses of vorinostat and givinostat

228 NOD mice receiving transient BAFF blockade were characte

229 ccurring islet-infiltrating B-lymphocytes in NOD mice recognizing the neuronal antigen peripherin.

230 expressing this ligand nonbinding isoform in NOD mice reduced IFN-gamma production in T effector cell

231 Thymi from different aged NOD mice, representing distinct stages of type 1 diabete

232 The ability of Tr1 cells to cure diabetes in NOD mice required IL-10 signaling, as Tr1 cells could no

233 c-Rel-competent Treg cells from prediabetic NOD mice reversed the accelerated diabetes development i

234 Chemokine levels in prostate tissue from NOD mice showed increased expression levels of CXCR3 lig

235 4(+) and CD8(+) T cells from c-Rel-deficient NOD mice showed significantly decreased T-cell receptor-

236 anti-insulin B cells in H chain-only VH125Tg/NOD mice showed that BTK-dependent selection into the MZ

237 ell signaling, and its deletion in T1D-prone NOD mice significantly reduces diabetes.

238 NOD mice spontaneously develop type 1 diabetes like huma

239 Nonobese diabetic (NOD) mice spontaneously develop type 1 diabetes (T1D), p

240 Treatment of NOD mice starting at 10 wk of age, when the autoimmune p

241 CID recipients showed that only T cells from NOD mice successfully infiltrated the prostate.

242 within the polyclonal repertoire of VH125Tg/NOD mice, suggesting enhanced central tolerance by direc

243 on of PTPs and STAT1 signaling compared with NOD mice that do not have insulitis.

244 nce and glucose homeostasis were assessed in NOD mice that expressed mouse preproinsulin II from a tr

245 DCs in diabetes, we examined Batf3-deficient NOD mice that lacked the CD103(+) DCs in islets and panc

246 In this study, we generated transgenic NOD mice that overexpressed Pep in T cells.

247 NOD mice that received beta-cell-Ag-loaded, zymosan-expo

248 Pre-diabetic NOD mice that received injections of the deoxyhypusine i

249 Analysis of NOD mice that were deficient in MR1, and therefore lacke

250 Female NOD mice that were maintained on acidic pH water (AW) de

251 generated diabetes-prone non-obese diabetic (NOD) mice that express insulin, via a transgene, in K ce

252 etion (CD11cCreXDTA.B6 and CD11cCreRosa26DTA.NOD mice) that DCs play a crucial role in regulating Val

253 opment in a subset of proinsulin 2-deficient NOD mice, the activation of iNKT cells by a specific ago

254 In NOD mice, the autoimmune process imparted an increased i

255 pressed in SG inflammatory foci in the SG of NOD mice, the expression of soluble CD40:Fc did not lead

256 Importantly, therapeutic intervention in NOD mice through nutritional supplementation or lentivir

257 Accordingly, mixed chimerism was induced in NOD mice through radiation-free nonmyeloablative anti-CD

258 diabetes (Idd) loci predisposing humans and NOD mice to disease.

259 We generated c-Rel-deficient NOD mice to examine the role of c-Rel in the development

260 proteomic analyses revealed NOD and Ealpha16/NOD mice to host mild but significant differences in the

261 cells from the BDC2.5 mouse into prediabetic NOD mice to mimic a physiological precursor frequency an

262 o rapid type 1 diabetes (T1D) development in NOD mice transgenic for the BDC2.5 T-cell receptor.

263 Thus, we generated and characterized NOD mice transgenically expressing an Ig molecule repres

264 NOD mice transgenically expressing Ig molecules recogniz

265 lyclonal splenocytes from nonobese diabetic (NOD) mice transplacentally treated with PPI-Fc were less

266 Despite the absence of diabetes, NOD mice treated with anti-CSF-1 receptor starting at 3

267 NOD mice treated with AZD1480 were protected from autoim

268 with increased frequency in the periphery of NOD mice versus nonautoimmune C57BL/6 VH125Tg mice; howe

269 When acutely administered by injection into NOD mice via the tail vein, this FSI formulation signifi

270 entral tolerance to proinsulin in transgenic NOD mice was broken on a granzyme A-deficient background

271 ore, DeltaT2 of the pancreata of prediabetic NOD mice was significantly higher than that of diabetic

272 + T cells, but not serum, from CP-1-infected NOD mice was sufficient to induce chronic pelvic pain.

273 To test this hypothesis, female NOD mice were administered pioglitazone during the pre-d

274 Brains of young and adult female NOD mice were examined, but young NOD mice did not displ

275 out clinical toxicity, whereas AhR-deficient NOD mice were not protected.

276 When prediabetic NOD mice were treated with 2-deoxyglucose to block aerob

277 NOD mice were treated with a combination of IL-2/anti-IL

278 Pregnant nonobese diabetic (NOD) mice were fed a GF or standard diet until all pups

279 ry vitamin D3 can safely prevent diabetes in NOD mice when administered lifelong, although caution is

280 irt6 abundance is found in the hyperglycemic NOD mice, which might increase DNA damage repair.

281 complex potently protects nonobese diabetic (NOD) mice, which normally lack this isotype, from sponta

282 /6 and autoimmunity-prone nonobese diabetic (NOD) mice, which show ineffective ERK activation after T

283 lin was ineffective in reversing diabetes in NOD mice whose glycemia was controlled with SC insulin p

284 In addition, treatment of NOD mice with 2-deoxyglucose resulted in improved beta c

285 Treatment of C57BL/6 or NOD mice with a monoclonal antibody to the CSF-1 recepto

286 es incidence in 125Tg/NOD mice as it does in NOD mice with a normal B cell repertoire.

287 ing polyneuropathy develops spontaneously in NOD mice with a partial loss of Aire function (NOD.Aire(

288 We conclude that treatment of NOD mice with an antibody against CSF-1 receptor reduced

289 Combination therapy of diabetic RIP-LCMV and NOD mice with anti-CD3 and anti-CXCL10 antibodies caused

290 Colonization of GF NOD mice with defined microbiota revealed that some, but

291 of new-onset mice and, remarkably, in 50% of NOD mice with established disease.

292 NOD mice with intestinal K cells engineered to express i

293 Here, we demonstrate that pancreata from NOD mice with islet infiltration have enhanced oxidation

294 Treatment of prediabetic NOD mice with low-dose beta-glucan resulted in a profoun

295 In this study, we treated NOD mice with new-onset as well as established disease u

296 was identified in crosses of T1D-susceptible NOD mice with the strongly T1D-resistant ALR strain.

297 model of chronic pelvic pain in NOD/ShiLtJ (NOD) mice with a clinical Escherichia coli isolate (CP-1

298 f a miRNA92a antagomir to nonobese diabetic (NOD) mice with ongoing islet autoimmunity resulted in a

299 d no evidence of methylene blue in the iliac nodes; mice without surgical intervention or with sham L

300 We conclude that in NOD mice, ZnT8 is a minor diabetogenic antigen that can