ライフサイエンスコーパス: NOD mice

1 unity after islet transplantation in ~50% of NOD mice.

2 teraction significantly delayed T1D onset in NOD mice.

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

4 d also strongly inhibited T1D development in NOD mice.

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

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

7 on and development of autoimmune diabetes in NOD mice.

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

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

10 eptor therapy reverses diabetes in new onset NOD mice.

11 pression is reduced in Valpha14iNKT cells of NOD mice.

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

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

14 ing early-onset autoimmune diabetogenesis in NOD mice.

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

16 erved in UBASH3A-deficient than in wild-type NOD mice.

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

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

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

20 ndividual islets of spontaneously autoimmune NOD mice.

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

22 and in preventing and reversing diabetes in NOD mice.

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

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

25 interferon regulatory factor 5 compared with NOD mice.

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

27 ti-insulin vaccine response in SAP-deficient NOD mice.

28 ed against spontaneous development of T1D in NOD mice.

29 equently an enduring reversal of diabetes in NOD mice.

30 treatment, prevents diabetes development in NOD mice.

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

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

33 pancreatic beta cells compared with control NOD mice.

34 red autoimmune response and T1D incidence in NOD mice.

35 es development in TLR4-deficient (TLR4(-/-)) NOD mice.

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

37 7 cells for stability and diabetogenicity in NOD mice.

38 vely restore normoglycemia in newly diabetic NOD mice.

39 ot prevent diabetes onset in immunocompetent NOD mice.

40 he initiation and progression of diabetes in NOD mice.

41 and reverse diabetes in newly hyperglycemic NOD mice.

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

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

44 nsistent feature of the islet infiltrates of NOD mice.

45 5 weeks of age]) safely prevents diabetes in NOD mice.

46 of thymic involution that is accelerated in NOD mice.

47 diabetes development in both male and female NOD mice.

48 to promote progression to overt diabetes in NOD mice.

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

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

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

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

53 dulates type 1 diabetes (T1D) progression in NOD mice.

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

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

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

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

58 ppressed late preclinical type 1 diabetes in NOD mice.

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

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

61 gen specificities and autoimmune diabetes in NOD mice.

62 es by targeting autoimmune CD4(+) T cells in NOD mice.

63 ype insulin-specific CD4(+) T and B cells in NOD mice.

64 previously shown to be protective of T1D in NOD mice.

65 (C57BL/6); and HLA-DQ8, huCD4 transgenic Ab0 NOD mice.

66 gression and rapid onset of hyperglycemia in NOD mice.

67 e increasing Treg activation in pancreata of NOD mice.

68 (Z-FL), was administered to 14-15 week male NOD mice.

69 egulatory T cells and serum soluble CD137 in NOD mice.

70 ground, designated as A22Calpha(-/-)PI2(-/-) NOD mice.

71 secretion and improved glucose tolerance in NOD mice.

72 served in wild-type, but not TLR2-deficient, NOD mice.

73 ajor contributors to autoimmune pathology in NOD mice.

74 ls and increased the number of beta cells in NOD mice.

75 to the tail pancreatic lymph node (TPLN) in NOD mice.

76 responses and promote beta cell survival in NOD mice.

77 induces psoriatic arthritis-like symptoms in NOD mice.

78 to BF on type 1 diabetes (T1D) incidence in NOD mice.

79 promising approach for diabetes reversal in NOD mice.

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

81 and diabetes was reversed in newly diagnosed NOD mice.

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

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

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

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

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

87 age in autoimmunity-prone nonobese diabetic (NOD) mice.

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

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

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

91 In polyclonal NOD mice, a high frequency (~40%) of HIP2.5-specific isl

92 LG acinar cells (LGAC)(p = 0.0026) from male NOD mice, a model of autoimmune dacryoadenitis in SS, re

93 and 3D genome organization in thymocytes of NOD mice, a model of type 1 diabetes (T1D), and the diab

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

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

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

97 In nonobese diabetic (NOD) mice, a model of T1D, diabetes development accelera

98 imal glands (LG) of male non-obese diabetic (NOD) mice, a murine model of SS.

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

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

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

102 utoimmune mice, a deficiency that worsens as NOD mice age toward diabetes and leaves them unable to r

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

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

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

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

107 t of IL-2, prevents the onset of diabetes in NOD mice and controls diabetes in hyperglycemic mice.

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

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

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

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

112 SAs promoted beta cell proliferation in both NOD mice and MIN6 cells and increased the number of beta

113 nd proconvertase-2 infiltrated the islets of NOD mice and transferred diabetes into NOD/scid recipien

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

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

116 ors for salivary gland dysfunction in female NOD mice, and might not be representative of the mechani

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

118 ested from 4 week-, 8 week-, and 12 week-old NOD mice, and their microvasculature, extracellular matr

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

120 CD4 responses in NOD mice are dominated by insulin epitope B:9-23 (InsB(9

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

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

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

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

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

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

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

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

129 des were administered to non-obese diabetic (NOD) mice at the onset of diabetes within two clinically

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

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

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

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

134 type 1 diabetes (T1D) in non-obese diabetic (NOD) mice but proved less effective in humans.

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

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

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

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

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

140 arrests beta-cell destruction in prediabetic NOD mice by generating InsB9-23-specific FoxP3(+) T regu

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

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

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

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

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

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

147 Diabetic NOD mice conditioned with CT25 when glycemia was <500 mg

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

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

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

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

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

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

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

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

156 l PAHSA administration to nonobese diabetic (NOD) mice delayed the onset of T1D and markedly reduced

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

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

159 In NOD mice depleted of islet-resident macrophages starting

160 accounts for our finding that CD70-deficient NOD mice develop more-aggressive T1D onset.

161 NOD mice develop spontaneous autoimmune type 1 diabetes

162 Consistently, UBASH3A-deficient NOD mice developed accelerated T1D in both sexes, which

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

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

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

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

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

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

171 Finally, we show that B cells in NOD mice express reduced PTEN, and low-dosage p110delta

172 Ins2-CCL21 transgenic, nonobese diabetic (NOD) mice express CCL21 in pancreatic beta-cells and do

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 -FL to a different cohort of 14-15 week male NOD mice for 6 weeks significantly reduced only tear CTS

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

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

182 Female NOD mice from The Jackson Laboratory (JAX) and Taconic B

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

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

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

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

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

188 Considering that NOD mice have been used to test numerous experimental th

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

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

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

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

193 Transgenic NOD mice in which Greater Amberjack fish (Seriola dumeri

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

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

199 ymocytes revealed that genomic misfolding in NOD mice is mediated in cis.

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 We determined that specific CD8 Tregs from NOD mice lack suppressive function, representing a previ

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

206 In this study, T-cell PTPN2 deficiency in NOD mice markedly accelerated the onset and increased th

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

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

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

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

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

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

213 s, this study investigated SS development in NOD mice obtained from two vendors.

214 Isolated pancreatic islets were derived from NOD mice of three distinct age groups (3, 8 and 18-week-

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

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

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

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

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 NOD mice possess 11-fold fewer Ly-49(+) CD8 Tregs than n

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

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

224 s in newly hyperglycemic non-obese diabetic (NOD) mice, protecting the insulin-producing beta-cells f

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

226 Weaning NOD mice received low doses of vorinostat and givinostat

227 NOD mice receiving Seriola dumerili transgenic islet tra

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 ncreased T-cells and macrophages, in LG from NOD mice relative to BALB/c.

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 he expression of miR-216a in the islets from NOD mice significantly changed during T1D progression.

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

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

242 granule proteins targeted in both humans and NOD mice supports their disease relevance and identifies

243 signaling, since PAHSAs lowered ER stress in NOD mice, suppressed thapsigargin-induced PARP cleavage

244 mation was markedly reduced in SAP-deficient NOD mice, T cells with a GC Tfh phenotype were found at

245 Relative to wild-type NOD mice, T1D development in the NOD.Tnfsf9 (-/-) strain

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

247 role of NKG2D in the pancreas, we generated NOD mice that express an NKG2D ligand in beta-islet cell

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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 ssfully targeted Tnfsf9 (encoding CD137L) in NOD mice using the CRISPR/Cas9 system (designated NOD.Tn

269 le of UBASH3A in T1D, we targeted Ubash3a in NOD mice using zinc-finger nuclease mediated mutagenesis

270 elivery of proinsulin in non-obese diabetic (NOD) mice using the coated MN system stimulated signific

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

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

273 Here, using BDC2.5 transgenic and NOD mice, we investigated T-cell recognition of the HIP2

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

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

276 lls (Tregs) can prevent T1D onset, groups of NOD mice were orally treated with Lactococcus lactis (LL

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

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

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

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

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

282 ng GC Tfh cells infiltrating the pancreas of NOD mice, which was enhanced by loss of SAP NOD T cells

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

284 /6 and autoimmunity-prone nonobese diabetic (NOD) mice, which show ineffective ERK activation after T

285 ated allogeneic C57BL/6 islets into diabetic NOD mice will prolong graft function and elicit localize

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

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

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

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

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

291 ystem, we treated the A22Calpha(-/-)PI2(-/-) NOD mice with enrofloxacin, a broad-spectrum antibiotic.

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

293 NOD mice with intestinal K cells engineered to express i

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

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

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

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

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