ライフサイエンスコーパス: NOD mouse

1 treat and cure type 1 diabetes (T1D) in the NOD mouse.

2 murine models of type 1 diabetes such as the NOD mouse.

3 regulator of diabetes susceptibility in the NOD mouse.

4 sease, parallel to prior observations in the NOD mouse.

5 genic CD4 Th1 T cell clones derived from the NOD mouse.

6 utoimmune diseases including diabetes in the NOD mouse.

7 or the development of type I diabetes in the NOD mouse.

8 e maturation of dendritic cells (DCs) in the NOD mouse.

9 mically induced diabetes pathogenesis in the NOD mouse.

10 stic of the SS-like phenotype present in the NOD mouse.

11 t cure of established type 1 diabetes in the NOD mouse.

12 s to escape thymic negative selection in the NOD mouse.

13 ly defined role in IDDM in humans and in the NOD mouse.

14 e CD4 T cell development/accumulation in the NOD mouse.

15 d from pancreatic beta-cells of a transgenic NOD mouse.

16 munity and destructive autoreactivity in the NOD mouse.

17 one during the development of disease in the NOD mouse.

18 ogenic or with their protective roles in the NOD mouse.

19 of autoimmune diabetes in the unmanipulated NOD mouse.

20 tive T cell repertoire in the diabetes-prone NOD mouse.

21 D4 T-cell reactivity to ZnT8 epitopes in the NOD mouse.

22 ms during the development of diabetes in the NOD mouse.

23 incorporates a strong immune phenotype: the NOD mouse.

24 critical in human type 1 diabetes and in the NOD mouse.

25 on but did not prevent or reverse T1D in the NOD mouse.

26 esults indicate that aPC prevents T1D in the NOD mouse.

27 uce rapid onset type 1 diabetes in the young NOD mouse.

28 ntial for the development of diabetes of the NOD mouse.

29 pecific model and the spontaneously diabetic NOD mouse.

30 e 1 diabetes (T1D) in the nonobese diabetic (NOD) mouse.

31 t causes diabetes of the non-obese diabetic (NOD) mouse.

32 y diabetic disease in the nonobese diabetic (NOD) mouse.

33 occurs in humans and the nonobese diabetic (NOD) mouse.

34 ets of Langerhans of the non-obese diabetic (NOD) mouse.

35 diabetes mellitus and the nonobese diabetic (NOD) mouse.

36 ns of mice, including the nonobese diabetic (NOD) mouse.

37 ncreas of the prediabetic nonobese diabetic (NOD) mouse.

38 of type 1 diabetes in the nonobese diabetic (NOD) mouse.

39 mp2 and Tap1 genes in the nonobese diabetic (NOD) mouse.

40 enesis of diabetes in the nonobese diabetic (NOD) mouse.

41 utoimmune diabetes of the nonobese diabetic (NOD) mouse.

42 e 1 diabetes (T1D) in the nonobese diabetic (NOD) mouse.

43 eous type 1 diabetes: the nonobese diabetic (NOD) mouse.

44 murine model of SS; the Non-Obese Diabetic (NOD) mouse.

45 produced a T-cell receptor (TCR) transgenic NOD mouse, 6.9TCR/NOD, in which the expression of both d

46 sion levels of >39,000 genes and ESTs in the NOD mouse (a murine model of T1D and other autoimmune co

47 In the NOD mouse, a causative link between increased expression

48 D25(+) T reg cells in the nonobese diabetic (NOD) mouse, a murine model for type 1 diabetes (T1D).

49 diabetogenic genes in the nonobese diabetic (NOD) mouse, a recombinational hotspot from the B10.A(R20

50 ould be reproduced in the nonobese diabetic (NOD) mouse, a spontaneous, chronic model of autoimmune d

51 NOD mouse AIP was associated with severe periductal and

52 he progression of autoimmune diabetes in the NOD mouse, an animal model of human type 1 diabetes.

53 ration on the development of diabetes in the NOD mouse and assessed whether this potential diabetes-s

54 Both the NOD mouse and human Deaf1 variant isoforms suppressed PT

55 ation of endogenous IL-10 was applied to the NOD mouse and indicated that IL-10 encounter with diabet

56 nd progression of autoimmune diabetes in the NOD mouse and provide the rationale to develop new thera

57 itic cells (mcDCs), are more numerous in the NOD mouse and, when Ag-loaded, rescue CD8(+) T cells fro

58 IL-21 was observed in the nonobese diabetic (NOD) mouse and suggested to contribute to diabetes by au

59 t proinsulin is a primary autoantigen of the NOD mouse, and speculate that organ-restricted autoimmun

60 mocytes as well as peripheral T cells in the NOD mouse, and we report further that A.SW mice demonstr

61 The NOD mouse appears to be a valuable model of diabetic sym

62 pancreatic islets in the nonobese diabetic (NOD) mouse are still unknown.

63 Type 1 diabetes in the nonobese diabetic (NOD) mouse arises as a consequence of T cell-mediated de

64 ed in clinical trials, seems to validate the NOD mouse as a meaningful model for the study of therape

65 Given the importance of the NOD mouse as a model of type 1 diabetes, there is a surp

66 on of disease-modifying agents tested in the NOD mouse based on treatment timing, duration, study len

67 ells are required for type 1 diabetes in the NOD mouse, because engineered mice lacking this populati

68 hereby may contribute to the pathogenesis of NOD mouse beta-cells.

69 LVA calcium channels abnormally expressed in NOD mouse beta-cells.

70 These results suggest that in the NOD mouse, beta-cell destruction begins soon after the o

71 DCs propagated from NOD mouse bone marrow and treated with NF-kappaB-specifi

72 in D3 [1,25(OH)2D3], prevent diabetes in the NOD mouse but also elicit unwanted calcemic side effects

73 frsf9 (encoding CD137/4-1BB) directly in the NOD mouse by embryo microinjection.

74 G-CSF prevents type 1 diabetes in the NOD mouse by promoting the local recruitment of T regula

75 portant role in the initiation of T1D in the NOD mouse by regulating the maturation of DCs and, thus,

76 ells (DC) in type 1 diabetes mellitus of the NOD mouse by using diphtheria toxin-mediated cell ablati

77 x that is highly unfavorable for a subset of NOD mouse CD4 cells, thereby greatly enhancing their res

78 r the reduced male incidence of IDDM in some NOD mouse colonies.

79 ever, we report that Tbx21 deficiency in the NOD mouse completely blocks insulitis and diabetes due t

80 n studies pertaining to T1D; descriptions of NOD mouse congenic strains; the Beta Cell Gene Expressio

81 Thus, the B7-2-deficient NOD mouse constitutes the first model of a spontaneous a

82 Our previous data in the NOD mouse demonstrated that co-administration of antigen

83 e receptor, KIR3DL1, in a nonobese diabetic (NOD) mouse-derived autoantigen-specific Treg (2D2), whic

84 The NOD mouse develops T1D spontaneously and serves as an an

85 nt of autoimmune inflammatory disease in the NOD mouse disease model.

86 n late stages of diabetes development in the NOD mouse-disease transferred with diabetogenic T cells

87 on of IDO-expressing islets from prediabetic NOD mouse donors into NODscid recipient mice is associat

88 odies (IAA) between 3 and 5 wk of age in the NOD mouse (early-IAA (E-IAA)).

89 B cell depletion, we generated a transgenic NOD mouse expressing human CD20 (hCD20) on B cells.

90 atic islets, protects the nonobese diabetic (NOD) mouse from insulin-dependent diabetes mellitus (IDD

91 In the nonobese diabetic (NOD) mouse, genetic deletion of the Ifng or the Il12b (I

92 ns that predispose to type 1 diabetes in the NOD mouse have been dissected, it has become apparent th

93 ine susceptibility to type 1 diabetes in the NOD mouse have been mapped to chromosome 1, Idd5.1 (insu

94 ype 1 diabetic humans and macrophages of the NOD mouse have markedly elevated autocrine GM-CSF produc

95 APCs of the nonobese diabetic (NOD) mouse have a genetically programmed capacity to ove

96 animal models such as the nonobese diabetic (NOD) mouse have improved our understanding of disease pa

97 ial age-dependent effects on diabetes in the NOD mouse; (iii) CD4+CD25+ T cells from NOD mice treated

98 ully manifested the SS-like phenotype of the NOD mouse, including decreased salivary and lacrimal gla

99 ental manipulations of the NKT defect in the NOD mouse induced corresponding changes in disease.

100 hAAT vector or with serum of hAAT transgenic NOD mouse induced immune tolerance to rAAV1-hAAT injecti

101 The NOD mouse is a model for autoimmune type 1 diabetes in h

102 The NOD mouse is a model of human IDDM, which is characteriz

103 The NOD mouse is a spontaneous T1D model that shares with hu

104 The NOD mouse is an animal model of IDDM that shows many of

105 The NOD mouse is an invaluable model for the study of autoim

106 hat islet allograft survival in the diabetic NOD mouse is determined by the interplay of diverse isle

107 The NOD mouse is genetically predisposed to the development

108 ance to allograft tolerance induction in the NOD mouse is not a direct consequence of overt autoimmun

109 ich the antigen locus on chromosome 6 of the NOD mouse is replaced by a segment from BALB/c.

110 The nonobese diabetic (NOD) mouse is a good model for human type 1 diabetes, wh

111 The nonobese diabetic (NOD) mouse is a well-established mouse model of spontane

112 The nonobese diabetic (NOD) mouse is an animal model of human type I diabetes w

113 diabetes mellitus in the nonobese diabetic (NOD) mouse is not well understood.

114 of type 1 diabetes in the nonobese diabetic (NOD) mouse is preceded by an immune cell infiltrate in t

115 utoimmune diabetes in the nonobese diabetic (NOD) mouse is under the control of multiple insulin-depe

116 he cytotoxic effect of CD8(+) T-cells toward NOD mouse islets.

117 ced iNOS expression and nitrite formation by NOD mouse islets.

118 N-gamma) to prime rat and nonobese diabetic (NOD) mouse islets for interleukin-1 (IL-1)-stimulated ex

119 sequent inflammatory insulitis in non-obese (NOD) mouse islets, we examined the T cell receptor TCR V

120 ATH) activities were significantly higher in NOD mouse LG lysate than in control lysates, and CATS wa

121 pare the gene expression in 12-week-old male NOD mouse LG relative to that in matched BALB/c mouse LG

122 nd CD68-positive infiltrating macrophages in NOD mouse LG.

123 y characterizing gene expression profiles of NOD mouse LGs in comparison with those of healthy contro

124 type 1 diabetes using a previously reported NOD mouse line expressing an Ealpha transgene and, there

125 s at different ages in GAD-tg mice and their NOD mouse littermates.

126 GIMAP5 has a key role in BB-DR rat and NOD mouse lymphopenia.

127 ension analysis shows that WE14 bound to the NOD mouse major histocompatibility complex class II mole

128 These data suggest that the NOD mouse may be a good candidate to study an interface

129 of the challenges for researchers using the NOD mouse model (and, indeed, other models of spontaneou

130 reported achievement of both advances in the NOD mouse model by coupling injection of Freund's comple

131 ression to autoimmune diabetes in the BDC2.5/NOD mouse model by reining in natural killer (NK) cells

132 With the NOD mouse model closely mimicking the human disease, our

133 similar alterations in CD73 in the NY8.3 TCR NOD mouse model crossed with TLR9(-)/(-) mice and by the

134 in-dependent diabetes mellitus (IDDM) in the NOD mouse model entails MHC class I-restricted CD8 T cel

135 To assess the value of the NOD mouse model for the evaluation of treatments relevan

136 ich carry diverse TCRs, prevented T1D in the NOD mouse model for the human disease.

137 Type 1 diabetes in the NOD mouse model has been linked to >30 insulin-dependent

138 contribute to diabetes susceptibility in the NOD mouse model have been identified, but only 2 chromos

139 A series of recent studies in humans and the NOD mouse model have highlighted the central role that a

140 reatments for type 1 diabetes studied in the NOD mouse model have not been replicated in human diseas

141 leading to autoimmune type 1 diabetes in the NOD mouse model involves at least 19 genetic loci.

142 Type 1 diabetes development in the NOD mouse model is widely reported to be dependent on hi

143 In the NOD mouse model of autoimmune diabetes, several beta cel

144 d the impact of granzyme A deficiency in the NOD mouse model of autoimmune diabetes.

145 mediator of thymocyte deletion, BIM, in the NOD mouse model of autoimmune diabetes.

146 fically ablated Foxp3(+) cells in the BCD2.5/NOD mouse model of autoimmune diabetes.

147 Human DQ8 and I-A(g7), in the NOD mouse model of spontaneous autoimmune diabetes, conf

148 ized pancreas-infiltrating Treg cells in the NOD mouse model of T1D and uncovered a substantial enric

149 hed donors could reverse autoimmunity in the NOD mouse model of T1D.

150 apies for reversing new-onset disease in the NOD mouse model of T1D.

151 Investigations employing the NOD mouse model of the disease have revealed an essentia

152 ens, are required for T1D development in the NOD mouse model of the disease, and CD8(+) T cells speci

153 or the development of type 1 diabetes in the NOD mouse model of the disease.

154 be exploited to modulate autoimmunity in the NOD mouse model of type 1 diabetes (T1D).

155 itope for diabetogenic CD4(+) T cells in the NOD mouse model of type 1 diabetes (T1D).

156 Current reports in the NOD mouse model of type 1 diabetes are in conflict as to

157 In the NOD mouse model of type 1 diabetes, insulin-dependent di

158 d activation of insulin-specific CTLs in the NOD mouse model of type 1 diabetes.

159 d in many autoimmune diseases, including the NOD mouse model of type 1 diabetes.

160 The NOD mouse model recapitulates multiple features of human

161 In this study, we used the NOD mouse model to analyze what regulates NKT17 cell fre

162 MLD) streptozotocin (STZ) injections and the NOD mouse model to investigate the potency of CXCR1/2 in

163 function after transplantation, we used the NOD mouse model to study oxidative stress encountered du

164 tudy, we analyzed the immune response in the NOD mouse model to the neuronal protein peripherin (PRPH

165 Evidence is strongest for the NOD mouse model where blocking immune responses to insul

166 Similar effects were seen in the NOD mouse model, and in these mice, 1 week of treatment

167 +) T-cell receptor transgenic variant of the NOD mouse model, in which diabetes can be synchronously

168 In the NOD mouse model, PD-L1 regulates the development of diab

169 In this study in the NOD mouse model, we found that infection with a pancreat

170 eactive cells, fulfill these criteria in the NOD mouse model.

171 lopment and onset of SjS-like disease in the NOD mouse model.

172 he clinical phase of SjS-like disease in the NOD mouse model.

173 for autoimmune type 1 diabetes (T1D) in the NOD mouse model.

174 fective in preventing type 1 diabetes in the NOD mouse model.

175 islet allograft survival in the challenging NOD mouse model.

176 ons underlying the development of T1D in the NOD mouse model.

177 development of type 1 diabetes (T1D) in the NOD mouse model.

178 on induction inhibits T1D development in the NOD mouse model.

179 g the pathology of type 1 diabetes using the NOD mouse model.

180 to development of autoimmune diabetes of the NOD mouse model.

181 tes mellitus in both the non-obese diabetic (NOD) mouse model and humans.

182 region to diabetes in the nonobese diabetic (NOD) mouse model make LCK a premier candidate for a susc

183 Using a nonobese diabetic (NOD) mouse model of human type 1 diabetes, we investigat

184 enesis of diabetes in the nonobese diabetic (NOD) mouse model of IDDM is thought to be a T-cell-media

185 creatic beta cells in the nonobese diabetic (NOD) mouse model of insulin-dependent diabetes mellitus

186 e T cell responses in the nonobese diabetic (NOD) mouse model of spontaneous autoimmune diabetes.

187 L1 in SS pathogenesis in non-obese diabetic (NOD) mouse model of this disease.

188 se gene 88 (MyD88) in the nonobese diabetic (NOD) mouse model of type 1 diabetes (T1D) results in mic

189 In the nonobese diabetic (NOD) mouse model of type 1 diabetes (T1D), an insulin pe

190 sing hyperglycemia in the nonobese diabetic (NOD) mouse model of type 1 diabetes (T1D), yet situation

191 for CD4(+) T cells in the nonobese diabetic (NOD) mouse model of type 1 diabetes (T1D).

192 at revert diabetes in the nonobese diabetic (NOD) mouse model of type 1 diabetes and counteract infla

193 cus linkage data from the nonobese diabetic (NOD) mouse model of type 1 diabetes has previously provi

194 In the nonobese diabetic (NOD) mouse model of type 1 diabetes, the immune system r

195 In the nonobese diabetic (NOD) mouse model of type 1 diabetes, we have identified

196 vert hyperglycemia in the nonobese diabetic (NOD) mouse model of type 1 diabetes.

197 yte/endothelial interactions in the NOD/LtJ (NOD) mouse model of type 1 diabetes.

198 Further, in the non-obese diabetic (NOD) mouse model of type I diabetes, encapsulated primar

199 al experiments using the non-obese diabetic (NOD) mouse model reported mucosal administration of T1D-

200 ve been implicated in the nonobese diabetic (NOD) mouse model, few causal gene variants have been ide

201 d the clinically relevant nonobese diabetic (NOD) mouse model.

202 o prevent diabetes in the nonobese diabetic (NOD) mouse model.

203 ype 1 diabetes using the non-obese diabetic (NOD) mouse model.

204 hyperglycemia in Lnglc human CD20 transgenic NOD mouse models.

205 cells cloned from the spontaneously diabetic NOD mouse more closely resemble effector T cells arising

206 r loss of beta-cell mass and function in the NOD mouse occurs gradually, beginning after the onset of

207 elop in the superior cervical ganglia of the NOD mouse or in the SMG-CG of non-diabetic NOD siblings.

208 a spontaneously diabetic nonobese diabetic (NOD) mouse or the NOD-derived, diabetogenic CD4(+) T cel

209 oncentration was two- to threefold higher in NOD mouse pancreatic beta-cells compared with Swiss-Webs

210 mokine CCL22 in pancreatic beta cells in the NOD mouse prevents autoimmune attack by recruiting T reg

211 n these results, we propose that IDDM in the NOD mouse progresses as a predominant inflammatory beta-

212 The percentage of NOD mouse recipients (8 wk of age) that engrafted with d

213 hed normal BALB/c and spontaneously-diabetic NOD mouse recipients.

214 diated rejection of islet grafts in diabetic NOD mouse recipients.

215 ended backcrossing of this mouse line to the NOD mouse resulted in a segregation of the IFN-gammaR-de

216 ion started at an early disease stage in the NOD mouse resulted in significant protection from diabet

217 utoimmune diabetes in the nonobese diabetic (NOD) mouse results from a breakdown in tolerance to panc

218 cells to prevent autoimmune diabetes in the NOD mouse (see the related article beginning on page 225

219 and an animal model, the nonobese diabetic (NOD) mouse, show morphological and functional abnormalit

220 -cell clone, G9C8, in the nonobese diabetic (NOD) mouse, specific to low-avidity insulin peptide B15-

221 The culture of NOD mouse spleen cells with aPC reduced the secretion of

222 were isolated from diabetic and nondiabetic NOD mouse splenocytes and treated in the absence or pres

223 The defect in proteasome function in NOD mouse splenocytes was evident from impaired NF-kappa

224 The nonobese diabetic (NOD) mouse spontaneously develops T cell-dependent autoi

225 Type-1 diabetes in the nonobese diabetic (NOD) mouse starts with an insulitis stage, wherein a mix

226 The NOD mouse strain is an excellent model of autoimmune dis

227 The NOD mouse strain spontaneously develops autoimmune diabe

228 The nonobese diabetic (NOD) mouse strain has a genetic deficiency in natural ki

229 autoimmune diabetes-prone nonobese diabetic (NOD) mouse strain, deficient in B7-2 costimulation, is p

230 Ag7 molecule, such as the nonobese diabetic (NOD) mouse strain, which spontaneously develops autoimmu

231 the unique biology of the nonobese diabetic (NOD) mouse strain.

232 vitro experiments and in vivo analyses using NOD mouse strains was conducted to test the effect of re

233 to type 1 diabetes development in human and NOD mouse studies.

234 tes prior to autoimmune exocrinopathy in the NOD mouse suggests that it is an excellent model of seco

235 P3(+)RORgammat(+) intermediates arise in the NOD mouse T cell repertoire prior to inflammation and ca

236 ation of T cells, and a very small number of NOD mouse T cells may represent BDC2.5-like cells.

237 suppress the in vitro proliferation of other NOD mouse T cells without cell-cell contact.

238 ection of responses in the 1st International NOD Mouse T-Cell Workshop.

239 and CATS was also significantly elevated in NOD mouse tears.

240 immunodominant T-cell target antigen in the NOD mouse that plays a critical role in the disease proc

241 he first specific mutation in the MHC of the NOD mouse that specifically impacts the activity of gene

242 pontaneous animal model of this disease, the NOD mouse, the genes of the MHC play an important role i

243 In the nonobese diabetic (NOD) mouse, there exists a defect in APC function charac

244 esentation in the autoimmune diabetes of the NOD mouse: they do this by presenting peptides derived f

245 The NOD mouse thus provides an excellent model for the inves

246 We used the NOD mouse to assess the effect of targeting the T-lympho

247 hat the T-cell proliferation response of the NOD mouse to both native and denatured forms of the anti

248 We analyzed B cell kinetics in the NOD mouse to establish whether these checkpoints are int

249 have been examined in the nonobese diabetic (NOD) mouse; uncertainty remains about beta-cell dynamics

250 DNA binding domain in the nonobese diabetic (NOD) mouse was shown to have weaker DNA binding compared

251 sease pathogenesis in the nonobese diabetic (NOD) mouse, was used to investigate the possible mechani

252 betogenic CD4 T cell clones derived from the NOD mouse, we recently identified the beta cell secretor

253 l of type 1 diabetes, the nonobese diabetic (NOD) mouse, we found that insulin resistance driven by l

254 opment of diabetes in the nonobese diabetic (NOD) mouse, we used DNA microarrays to analyze gene expr

255 solated from the islets of a 5-wk-old female NOD mouse, which is capable of mediating overt diabetes

256 -specific CD4+ T-cell clone derived from the NOD mouse whose natural target antigen is unknown.

257 We initiated studies of APC function in the NOD mouse with respect to antigen processing and present

258 ween the MHC class I K and class II A of the NOD mouse with the recombinational site centromeric to t

259 in the development of type I diabetes in the NOD mouse, with obvious potential implications for type