ライフサイエンスコーパス: nonobese diabetic

1 ffect of actopaxin repression was studied in nonobese diabetic and severe combined immunodeficient mi

2 ls, we developed a novel nTreg model on pure nonobese diabetic background using epigenetic reprogramm

3 s were cotransferred into islet transplanted nonobese diabetic background with severe combined immuno

4 of the targeting (particularly strong on the nonobese diabetic background, but very mild on the C57BL

5 In contrast, in Th1-mediated diabetes, nonobese diabetic CD43(-/-) mice did not significantly d

6 This is demonstrated genetically in nonobese diabetic-gld/+ mice and pharmacologically by us

7 wild-type or IGRP(2)(0)(6)(-)(2)(1)(4)(-/-) nonobese diabetic hosts (harboring either naive and memo

8 his issue, we generated transgenic NOD mice (nonobese diabetic) in which Ptpn22 can be inducibly sile

9 implanted human breast cancer cell lines in nonobese diabetic/LtSz-scid/scid beta2 microglobulin-def

10 tigen-presenting cells, to treat diabetes in nonobese diabetic mice after disease onset.

11 vation and whose adoptive transfer protected nonobese diabetic mice against type 1 diabetes (T1D).

12 Thus, male nonobese diabetic mice allow for translational studies o

13 Gastric emptying was measured in nonobese diabetic mice and correlated with levels of HO-

14 oth muscle, and neurons were investigated in nonobese diabetic mice and organotypic cultures by immun

15 Autoimmune-prone nonobese diabetic mice deficient for B7-2 spontaneously

16 Studies of nonobese diabetic mice demonstrated that disruption of t

17 nce of type 1 diabetes (T1D) is decreased in nonobese diabetic mice expressing the complete cassette

18 Macrophage from nonobese diabetic mice failed to provide signals necessa

19 Fas (lpr) or FasL (gld) completely protects nonobese diabetic mice from autoimmune diabetes but also

20 n B13 autoantibodies in young diabetes-prone nonobese diabetic mice is associated with reduced inflam

21 CD4(+) T cells from JNK2-deficient nonobese diabetic mice produced less IFN-gamma but signi

22 tes-inducing CD4 T cell clones isolated from nonobese diabetic mice recognize epitopes formed by cova

23 e 1 or type 2 diabetes, and in the islets of nonobese diabetic mice that have developed insulitis or

24 sed Fah(-/-), Rag2(-/-), Il2r(-/-) mice with nonobese diabetic mice to create FRGN mice, whose livers

25 (Treg cells) during diabetes progression in nonobese diabetic mice was investigated to determine whe

26 xpression of NMI was detected in islets from nonobese diabetic mice with insulitis and in rodent or h

27 oliferation using in vivo teratoma assays in nonobese diabetic mice with severe combined immunodefici

28 In nonobese diabetic mice with uncontrolled type 1 diabetes

29 experimental autoimmune encephalomyelitis in nonobese diabetic mice, an experimental model that resem

30 In adult TCR (BDC2.5) transgenic nonobese diabetic mice, DNA microarray analysis of globa

31 In an alternative diabetes model, nonobese diabetic mice, IL15/IL-15Ralpha expression was

32 ccelerated BDC2.5 T-cell receptor transgenic nonobese diabetic mice, which experience development of

33 corticosterone were investigated using male nonobese diabetic mice.

34 otocin and during development of diabetes in nonobese diabetic mice.

35 tolerance and the development of diabetes in nonobese diabetic mice.

36 ng grafted and endogenous islets in diabetic nonobese diabetic mice.

37 antigen-specific Tregs from autoimmune-prone nonobese diabetic mice.

38 the onset and severity of type 1 diabetes in nonobese diabetic mice.

39 cell-specific injury or from the pancreas of nonobese diabetic mice.

40 ferred 5 x 10(6) splenocytes from 6-week-old nonobese diabetic mice.

41 oimmune diabetes developing spontaneously in nonobese diabetic mice.

42 ious studies in type 1 diabetes (T1D) in the nonobese diabetic mouse demonstrated that a crucial insu

43 The nonobese diabetic mouse model of human T1DM reveals that

44 In the nonobese diabetic mouse model of T1D, administration of

45 e in accord with prior observations from the nonobese diabetic mouse model, suggesting a mechanism sh

46 aluating these islets in immunocompetent and nonobese diabetic mouse models are underway.

47 Type 1 diabetes in the nonobese diabetic mouse stems from an infiltration of th

48 eta cells and the other using T cells in the nonobese diabetic mouse strain, which develops spontaneo

49 In the nonobese diabetic mouse, a predominant component of the

50 -DQ8 in man and the orthologous I-Ag7 in the nonobese diabetic mouse.

51 ts of diabetogenic CD4+ T cell clones in the nonobese diabetic mouse.

52 molecule alone in three lines of transgenic nonobese diabetic murine class II-deficient (mII(-/-)) m

53 In this study, we used immunocompetent nonobese diabetic (NOD) and immunocompromised NOD-scid-g

54 r organizing regions (NORs) in hyperglycemic nonobese diabetic (NOD) and old normoglycemic BALB/c mou

55 hese functions of B-cells, we have generated nonobese diabetic (NOD) B-cell-deficient mice that expre

56 utation of the Aire gene or substituting the nonobese diabetic (NOD) genetic background.

57 ted and preselected thymocytes, we show that nonobese diabetic (NOD) genetic variation impairs neithe

58 The compound immunodeficiencies in nonobese diabetic (NOD) inbred mice homozygous for the P

59 Additionally, 67% of TCRs cloned from nonobese diabetic (NOD) islet-infiltrating CD4(+) T cell

60 Four- to five-week-old female nonobese diabetic (NOD) littermates received intraperito

61 agement of TRPV1 can be transferred to naive nonobese diabetic (NOD) mice [model of type 1 diabetes (

62 Prediabetic nonobese diabetic (NOD) mice and control diabetes-resist

63 Idd5.1 regulates T1D susceptibility in nonobese diabetic (NOD) mice and has two notable candida

64 in beta cells isolated from islets of young nonobese diabetic (NOD) mice and nondiabetic mice as wel

65 o islet autoantigens, and that hyperglycemic nonobese diabetic (NOD) mice and T1D patients lack these

66 oides polygyrus, on type 1 diabetes (T1D) in nonobese diabetic (NOD) mice and to elucidate the mechan

67 has been suggested that diabetes-susceptible nonobese diabetic (NOD) mice are defective in the genera

68 k autoimmune diabetes, generally declines in nonobese diabetic (NOD) mice as disease progresses.

69 -dose-streptozotocin (MLDS) treatment and in nonobese diabetic (NOD) mice by cyclophosphamide injecti

70 of type 1 diabetes (T1D) can be prevented in nonobese diabetic (NOD) mice by reconstitution with auto

71 uction of islet transplantation tolerance in nonobese diabetic (NOD) mice can be reached by induction

72 ll peptide-pulsed dendritic cells (DCs) from nonobese diabetic (NOD) mice can effectively induce CD4(

73 found that the islets of Langerhans in young nonobese diabetic (NOD) mice contained two antigen-prese

74 d transplanted intraperitoneally in diabetic nonobese diabetic (NOD) mice given no immunosuppression

75 Nonobese diabetic (NOD) mice have a number of features t

76 Resting natural killer (NK) cells in nonobese diabetic (NOD) mice have impaired immune functi

77 Daily gavage of vehicle (dH2O) in nonobese diabetic (NOD) mice induced a social avoidance

78 eby B cells contribute to type 1 diabetes in nonobese diabetic (NOD) mice is as a subset of APCs that

79 to type 1 diabetes (T1D) in both humans and nonobese diabetic (NOD) mice is either promoted or domin

80 ring spontaneous type 1 diabetes mellitus in nonobese diabetic (NOD) mice is insulin.

81 In the current study, we demonstrate that nonobese diabetic (NOD) mice lacking expression of the M

82 e and human CD4 T cells isolated from either nonobese diabetic (NOD) mice or humans with T1D.

83 a (IL-7Ralpha) with monoclonal antibodies in nonobese diabetic (NOD) mice prevented autoimmune diabet

84 Nonobese diabetic (NOD) mice provide an excellent model

85 eatments that prevent autoimmune diabetes in nonobese diabetic (NOD) mice require intervention at ear

86 Type 1 diabetes in both humans and nonobese diabetic (NOD) mice results from autoreactive T

87 Nonobese diabetic (NOD) mice spontaneously develop type

88 Type 1 diabetes acceleration in nonobese diabetic (NOD) mice through coxsackievirus B4 (

89 However, we previously reported that nonobese diabetic (NOD) mice transgenic for a T cell ant

90 We generated Ab0 nonobese diabetic (NOD) mice transgenic for HLA-DR*0405,

91 Moreover, polyclonal splenocytes from nonobese diabetic (NOD) mice transplacentally treated wi

92 Pregnant nonobese diabetic (NOD) mice were fed a GF or standard d

93 Pretreatment of DCs prepared from nonobese diabetic (NOD) mice with AC blocked secretion o

94 al., and Suri et al. confirmed that treating nonobese diabetic (NOD) mice with an immune adjuvant and

95 Treatment of nonobese diabetic (NOD) mice with FTY720 before the deve

96 vivo application of a miRNA92a antagomir to nonobese diabetic (NOD) mice with ongoing islet autoimmu

97 In nonobese diabetic (NOD) mice with overt new-onset type 1

98 eviously reported that neonatal treatment of nonobese diabetic (NOD) mice with TNF-alpha accelerated

99 of families with a high incidence of T1D and nonobese diabetic (NOD) mice, a prototypical model of th

100 nt autoimmune diabetes in heavily irradiated nonobese diabetic (NOD) mice, a similar procedure is not

101 Os can stimulate the autoimmune responses in nonobese diabetic (NOD) mice, a spontaneous disease mode

102 y (T3A) was capable of systemic infection of nonobese diabetic (NOD) mice, an experimental model of a

103 6-67 of I-Abeta(g7) (I-A(b-g7)) in wild-type nonobese diabetic (NOD) mice, as well as NOD mice coexpr

104 ctive HDAC3 inhibitor, for 2 weeks to female nonobese diabetic (NOD) mice, beginning at 3 weeks of ag

105 en shown to delay this autoimmune disease in nonobese diabetic (NOD) mice, but the environmental cues

106 In specific pathogen-free nonobese diabetic (NOD) mice, females have 1.3-4.4 times

107 We demonstrated that in nonobese diabetic (NOD) mice, gal-1 therapy reduces sign

108 Despite widespread use of nonobese diabetic (NOD) mice, NOD with severe combined i

109 pendently two strains of mast cell-deficient nonobese diabetic (NOD) mice, NOD.Cpa3(Cre/+) (Heidelber

110 cephalomyelitis (EAE) and type I diabetes in nonobese diabetic (NOD) mice, repeated administration of

111 ld mutation) prevents autoimmune diabetes in nonobese diabetic (NOD) mice, the widely used model for

112 In nonobese diabetic (NOD) mice, two sets of autoreactive C

113 Nonobese diabetic (NOD) mice, which are used to model hu

114 with our in vitro findings, we observe that nonobese diabetic (NOD) mice, which express less IL-2 co

115 HC-II Ealpha:Ebeta complex potently protects nonobese diabetic (NOD) mice, which normally lack this i

116 poorly to the class II I-A(g7) molecules of nonobese diabetic (NOD) mice, which results in weak agon

117 cs in control C57BL/6 and autoimmunity-prone nonobese diabetic (NOD) mice, which show ineffective ERK

118 Macrophages from nonobese diabetic (NOD) mice, which spontaneously develo

119 T cells, which have demonstrated efficacy in nonobese diabetic (NOD) mice.

120 d the effects on autoimmunity in prediabetic nonobese diabetic (NOD) mice.

121 ive in ameliorating autoimmunity in diabetic nonobese diabetic (NOD) mice.

122 nset of destructive insulitis in the PLNs of nonobese diabetic (NOD) mice.

123 to reduced IL-4 production by CD4 cells from nonobese diabetic (NOD) mice.

124 ate rapid onset type 1 diabetes (T1D) in old nonobese diabetic (NOD) mice.

125 icroencapsulated porcine islet xenografts in nonobese diabetic (NOD) mice.

126 on of beta-cell function in overtly diabetic nonobese diabetic (NOD) mice.

127 ed T1D susceptibility interval (Idd4) in the nonobese diabetic (NOD) mice.

128 , is increased in islets from diabetes-prone nonobese diabetic (NOD) mice.

129 cDC1) DCs, respectively, in autoimmune-prone nonobese diabetic (NOD) mice.

130 the pathogenesis of type 1 diabetes (T1D) in nonobese diabetic (NOD) mice.

131 (HOT) on autoimmune diabetes development in nonobese diabetic (NOD) mice.

132 markers of the disease process in humans and nonobese diabetic (NOD) mice; however, the Ag-specific r

133 enerated Clec16a knock-down (KD) mice in the nonobese diabetic (NOD) model for type 1 diabetes and fo

134 ocus, and elevated IL-21 was observed in the nonobese diabetic (NOD) mouse and suggested to contribut

135 ne response against pancreatic islets in the nonobese diabetic (NOD) mouse are still unknown.

136 e 1 diabetes (T1D) animal models such as the nonobese diabetic (NOD) mouse have improved our understa

137 The nonobese diabetic (NOD) mouse is a well-established mous

138 Development of type 1 diabetes in the nonobese diabetic (NOD) mouse is preceded by an immune c

139 In the nonobese diabetic (NOD) mouse model of type 1 diabetes (

140 is an autoantigen for CD4(+) T cells in the nonobese diabetic (NOD) mouse model of type 1 diabetes (

141 tion primary response gene 88 (MyD88) in the nonobese diabetic (NOD) mouse model of type 1 diabetes (

142 effective at reversing hyperglycemia in the nonobese diabetic (NOD) mouse model of type 1 diabetes (

143 nostat and givinostat revert diabetes in the nonobese diabetic (NOD) mouse model of type 1 diabetes a

144 In the nonobese diabetic (NOD) mouse model of type 1 diabetes,

145 In the nonobese diabetic (NOD) mouse model of type 1 diabetes,

146 GCSF), to reverse overt hyperglycemia in the nonobese diabetic (NOD) mouse model of type 1 diabetes.

147 betes (Idd) loci have been implicated in the nonobese diabetic (NOD) mouse model, few causal gene var

148 (T1DM) in humans and the clinically relevant nonobese diabetic (NOD) mouse model.

149 he development of autoimmune diabetes in the nonobese diabetic (NOD) mouse results from a breakdown i

150 Type-1 diabetes in the nonobese diabetic (NOD) mouse starts with an insulitis s

151 The nonobese diabetic (NOD) mouse strain has a genetic defic

152 ype 1 diabetes via the unique biology of the nonobese diabetic (NOD) mouse strain.

153 tion in the Stat5b DNA binding domain in the nonobese diabetic (NOD) mouse was shown to have weaker D

154 nd quantify CD4(+)CD25(+) T reg cells in the nonobese diabetic (NOD) mouse, a murine model for type 1

155 rotective effects could be reproduced in the nonobese diabetic (NOD) mouse, a spontaneous, chronic mo

156 In the nonobese diabetic (NOD) mouse, genetic deletion of the I

157 1 diabetic patients and an animal model, the nonobese diabetic (NOD) mouse, show morphological and fu

158 diabetogenic CD8 T-cell clone, G9C8, in the nonobese diabetic (NOD) mouse, specific to low-avidity i

159 matical model of disease pathogenesis in the nonobese diabetic (NOD) mouse, was used to investigate t

160 In a model of type 1 diabetes, the nonobese diabetic (NOD) mouse, we found that insulin res

161 ls during the development of diabetes in the nonobese diabetic (NOD) mouse, we used DNA microarrays t

162 killer cell Ig-like receptor, KIR3DL1, in a nonobese diabetic (NOD) mouse-derived autoantigen-specif

163 development of type 1 diabetes (T1D) in the nonobese diabetic (NOD) mouse.

164 hat have cured early diabetic disease in the nonobese diabetic (NOD) mouse.

165 immune disease that occurs in humans and the nonobese diabetic (NOD) mouse.

166 molecules in the autoimmune diabetes of the nonobese diabetic (NOD) mouse.

167 D-1) constrains type 1 diabetes (T1D) in the nonobese diabetic (NOD) mouse.

168 ic model of spontaneous type 1 diabetes: the nonobese diabetic (NOD) mouse.

169 These processes have been examined in the nonobese diabetic (NOD) mouse; uncertainty remains about

170 erfamily 14 (TNFSF14) is upregulated in aged nonobese diabetic (NOD) pancreas with the appearance of

171 n predicted islet transplantation outcome in nonobese diabetic (NOD) scid mice (n=8).

172 All juvenile mice of the nonobese diabetic (NOD) strain develop insulitis, but th

173 itions are fulfilled in diabetic mice of the nonobese diabetic (NOD) strain.

174 eukocyte infiltration into the islets of the nonobese diabetic (NOD) type 1 diabetes-prone mouse mode

175 infiltrates of BDC2.5 transgenic mice on the nonobese diabetic (NOD) versus C57BL/6.H-2g7 genetic bac

176 -induced osteoclastogenesis and bone loss in nonobese diabetic (NOD) versus humanized NOD/SCID mice.

177 show that S. Typhi can replicate in vivo in nonobese diabetic (NOD)-scid IL2rgamma(null) mice engraf

178 Using nonobese diabetic (NOD)-scid IL2Rgammanull (NSG) mice re

179 Nonobese diabetic (NOD)-scid interleukin-2 gamma chain r

180 roach was validated by demonstrating that Rg nonobese diabetic (NOD)-scid mice expressing the diabeto

181 Nonobese diabetic (NOD)-scid-gammac(-/-) mice were injec

182 transplantation under the kidney capsule of nonobese diabetic (NOD)-severe combined immunodeficiency

183 ftment of primary human AML cells in vivo in nonobese diabetic (NOD)-severe combined immunodeficient

184 re combined immunodeficient (SCID)/Beige and nonobese diabetic (NOD)/SCID/IL-2gamma-receptor null (NS

185 ncture (CLP) in the severely immunodeficient nonobese diabetic (NOD)/SCID/IL2Rgamma(-/-) mice, and si

186 ymic tissue and CD34(+) fetal liver cells in nonobese diabetic (NOD)/severe combined immunodeficiency

187 cells (HSC) capable of serial engraftment in nonobese diabetic (NOD)/severe combined immunodeficient

188 ently demonstrated that superoxide-deficient nonobese diabetic (NOD.Ncf1(m1J)) mice exhibited a delay

189 notype of gastric macrophages in NOD/ShiLtJ (nonobese diabetic [NOD]) mice after onset of diabetes, w

190 found on insulin B:9-23-reactive T cells in nonobese diabetic rat islets.

191 tecting MIN6 cells in spontaneously diabetic nonobese diabetic recipients against both alloimmune and

192 ed into healthy HLA-DQ8(+)RAG-1(-/-)mII(-/-) nonobese diabetic recipients with lymphocytes, but not s

193 Nonobese diabetic RIP-IL35 transgenic mice exhibited dec

194 ing cells (SRCs) by transplantation into the nonobese diabetic SCID (NOD/SCID) mice; secondary transp

195 oad in the serum of human PBMC-reconstituted nonobese diabetic SCID mice by >6-fold.

196 ugs, and infection was fully resolved in 7/8 nonobese diabetic/SCID mice being infected with a multid

197 d a human (hu)RBC-SCID mouse model by giving nonobese diabetic/SCID mice daily transfusions of huRBCs

198 ancer cells were injected intrarectally into nonobese diabetic/SCID mice.

199 n in human hematopoietic stem cell-engrafted nonobese diabetic/SCID/IL-2Rgamma(null) mice: "human imm

200 ly image human immune cell reconstitution in nonobese diabetic severe combined immune deficiency gamm

201 HTLV-1-infected humanized nonobese diabetic severe combined immunodeficiency (HU-N

202 s or transplanted under the renal capsule of nonobese diabetic severe combined immunodeficiency (NOD

203 34(+) fetal liver cells into immunodeficient nonobese diabetic severe combined immunodeficiency (NOD/

204 Here, we show that nonobese diabetic severe combined immunodeficiency (NOD/

205 of streptozotocin (STZ)-induced diabetes in nonobese diabetic severe combined immunodeficiency (NOD/

206 Further, the nonobese diabetic severe combined immunodeficiency commo

207 ar morphology when transplanted with MSCs in nonobese diabetic severe combined immunodeficiency mice

208 Six nonobese diabetic severe combined immunodeficiency mice

209 specimens were implanted subcutaneously into nonobese diabetic severe combined immunodeficiency mice.

210 Humanized nonobese diabetic severe combined immunodeficient common

211 Nonobese diabetic severe combined immunodeficient gammac

212 In contrast to nonobese diabetic severe combined immunodeficient Il2rg(

213 Nonobese diabetic severe combined immunodeficient mice l

214 The chimeric nonobese diabetic severe combined immunodeficient mouse

215 escued lethal fulminant hepatic failure in a nonobese diabetic severe combined immunodeficient mouse

216 These investigations in a nonobese diabetic severe combined immunodeficient mouse-

217 capable of initiating highly invasive HCC in nonobese diabetic, severe combined immunodeficient mice.

218 mol/L) eradicated established tumors (ie, in nonobese diabetic-severe combined immunodeficiencies) th

219 an hepcidin or control tumor xenografts into nonobese diabetic-severe combined immunodeficiency (NOD-

220 of CD34+ cells with allogeneic T cells into nonobese diabetic-severe combined immunodeficiency (NOD/

221 and human CD34(+) cells that can repopulate nonobese diabetic-severe combined immunodeficiency (SCID

222 M2-like phenotype in vitro and in engrafted nonobese diabetic-severe combined immunodeficiency mice.

223 ocyte coculture and engraftment in NOD-SCID (nonobese diabetic-severe combined immunodeficiency) mous

224 Nonobese diabetic-severe combined immunodeficiency-gamma

225 epopulation in the marrow of immunodeficient nonobese diabetic-severe combined immunodeficient (NOD-S

226 regulatory proteins in the liver and gut of nonobese diabetic-severe combined immunodeficient (NOD/S

227 Stem cell engraftment into nonobese diabetic-severe combined immunodeficient (NOD/S

228 or assay) and implantation of these cells in nonobese diabetic-severe combined immunodeficient mice (

229 c immune responses following immunization of nonobese diabetic-severe combined immunodeficient mice t

230 f retinal ischemia-reperfusion-injured adult nonobese diabetic-severe combined immunodeficient mice.

231 ls alters mammary development in a humanized nonobese diabetic-severe combined immunodeficient mouse

232 To address this we used nonobese diabetic-severe combined immunodeficient-beta(2

233 ony-forming unit assays, flow cytometry, and nonobese diabetic/severe combined immune deficienct mous

234 othelial selectins in bone marrow vessels of nonobese diabetic/severe combined immune deficiency (NOD

235 event engraftment of human acute leukemia in nonobese diabetic/severe combined immune deficient mice,

236 ntravenous injection of karpas299 cells into nonobese diabetic/severe combined immuno-deficient (SCID

237 e human bipotential CD34(+) progenitors into nonobese diabetic/severe combined immunodeficiency (NOD-

238 PSMA-overexpressing tumors in nonobese diabetic/severe combined immunodeficiency (NOD/

239 (FA-A), we show that when transplanted into nonobese diabetic/severe combined immunodeficiency (NOD/

240 combination with daclizumab was evaluated in nonobese diabetic/severe combined immunodeficiency (NOD/

241 x vivo in culture and after engraftment in a nonobese diabetic/severe combined immunodeficiency (NOD/

242 In addition, we demonstrate that nonobese diabetic/severe combined immunodeficiency (NOD/

243 short-term repopulation assays performed on nonobese diabetic/severe combined immunodeficiency (NOD/

244 se-expressing Burkitt lymphoma xenografts in nonobese diabetic/severe combined immunodeficiency (NOD/

245 Nonobese diabetic/severe combined immunodeficiency (NOD/

246 al cell adhesion, homing, and engraftment in nonobese diabetic/severe combined immunodeficiency IL-2g

247 Nonobese diabetic/severe combined immunodeficiency mice

248 n vivo after transplantation in xenotolerant nonobese diabetic/severe combined immunodeficiency mice

249 ells, and significantly improved survival of nonobese diabetic/severe combined immunodeficiency mice

250 Transplantation of human erythrocytes into nonobese diabetic/severe combined immunodeficiency mice

251 r tissues and CD34(+) fetal liver cells into nonobese diabetic/severe combined immunodeficiency mice

252 und that primary ALL cells transplanted onto nonobese diabetic/severe combined immunodeficiency mice

253 eal injection of ex vivo leukemic cells into nonobese diabetic/severe combined immunodeficiency mice.

254 rmal lymphoid phenotype when transplanted to nonobese diabetic/severe combined immunodeficiency mice.

255 he most primitive assayable human cells, the nonobese diabetic/severe combined immunodeficiency mouse

256 Using a nonobese diabetic/severe combined immunodeficiency mouse

257 Therefore, we created a nonobese diabetic/severe combined immunodeficiency/inter

258 in vitro and reconstitute immune-deficient (nonobese diabetic/severe combined immunodeficiency/inter

259 ematopoietic reconstitution by transplanting nonobese diabetic/severe combined immunodeficiency/inter

260 is disease, in syngeneic hosts as well as in nonobese diabetic/severe combined immunodeficiency/inter

261 Tumor regression was blocked in nonobese diabetic/severe combined immunodeficient (NOD/S

262 n of systemic CD19(+) B-cell malignancies in nonobese diabetic/severe combined immunodeficient (NOD/S

263 We examined whether the nonobese diabetic/severe combined immunodeficient (NOD/s

264 A nonobese diabetic/severe combined immunodeficient (NOD/S

265 heir homing to the marrow and the spleens of nonobese diabetic/severe combined immunodeficient (NOD/S

266 n soft agar, and increased tumorigenicity in nonobese diabetic/severe combined immunodeficient (NOD/S

267 hypothesis using multiple ALL cell lines and nonobese diabetic/severe combined immunodeficient (NOD/S

268 al to generation of leukemia and survival in nonobese diabetic/severe combined immunodeficient (NOD/S

269 gical specimens or xenografts established in nonobese diabetic/severe combined immunodeficient (NOD/S

270 growth, lines were selected for passage into nonobese diabetic/severe combined immunodeficient (NOD/S

271 However, when injected into the nonobese diabetic/severe combined immunodeficient (NOD/S

272 To investigate the in vivo efficacy, nonobese diabetic/severe combined immunodeficient (NOD/S

273 al ALL cell lines and primary ALL samples in nonobese diabetic/severe combined immunodeficient (NOD/S

274 e introduced into the retroorbital plexus of nonobese diabetic/severe combined immunodeficient (NOD/S

275 lony assays, as well as stem cells using the nonobese diabetic/severe combined immunodeficient (NOD/S

276 ly decreased the engraftment of AML cells in nonobese diabetic/severe combined immunodeficient (NOD/S

277 The nonobese diabetic/severe combined immunodeficient (NOD/S

278 Here we report that a new nonobese diabetic/severe combined immunodeficient (NOD/S

279 IM CD34(+) cells engrafted nonobese diabetic/severe combined immunodeficient (NOD/S

280 t comparison of repopulation with use of the nonobese diabetic/severe combined immunodeficient (NOD/S

281 subtypes supported higher tumor incidence in nonobese diabetic/severe combined immunodeficient (NOD/S

282 or multifocally in the peritoneal cavity of nonobese diabetic/severe combined immunodeficient (NOD/S

283 treated JAK2V617F(+) PMF CD34(+) cells into nonobese diabetic/severe combined immunodeficient (SCID)

284 iated by these antibodies on an ATL model in nonobese diabetic/severe combined immunodeficient (SCID/

285 ansduced rat islets to restore euglycemia in nonobese diabetic/severe combined immunodeficient diabet

286 In nonobese diabetic/severe combined immunodeficient mice b

287 When IMC-EB10 was used in vivo to treat nonobese diabetic/severe combined immunodeficient mice g

288 ctor T cells when implanted as xenografts in nonobese diabetic/severe combined immunodeficient mice i

289 eritoneal dissemination of SKOV3ip1 cells in nonobese diabetic/severe combined immunodeficient mice,

290 nd promote the engraftment of these cells in nonobese diabetic/severe combined immunodeficient mice.

291 s and in vivo by competitive repopulation of nonobese diabetic/severe combined immunodeficient mice.

292 gh CXCR4/CXCL12 signals as shown in chimeric nonobese diabetic/severe combined immunodeficient mice.

293 oneal injection of MET-1 leukemic cells into nonobese diabetic/severe combined immunodeficient mice.

294 2,13-desoxyepothilone B (dEpoB) in xenograft nonobese diabetic/severe combined immunodeficient mouse

295 homing of human B cells, using a xenogeneic nonobese diabetic/severe combined immunodeficient mouse

296 We used the beta-glucuronidase-deficient nonobese diabetic/severe combined immunodeficient/mucopo

297 We demonstrate that nonobese diabetic/severely compromised immunodeficient (

298 d formed teratomas with three germ layers in nonobese diabetic/severely compromised immunodeficient m

299 NOD.c3c4 mice congenically derived from the nonobese diabetic strain develop an autoimmune biliary d

300 ts of Langerhans and is recapitulated in the nonobese diabetic strain of mice.