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 ntly faster and larger in SD-RG rats than in nonobese diabetic- Cg-Prkdc(scid) Il2rg(tm1Wjl)/SzJ mice

7 Nonobese diabetic/DQ8 mice were sensitized to gluten and

8 2(-/-) , and Il2rg(-/-) knockout mice on the nonobese diabetic (FRGN) background were repopulated wit

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

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

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

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

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

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

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

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

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

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

19 Studies of nonobese diabetic mice demonstrated that disruption of t

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

21 Macrophage from nonobese diabetic mice failed to provide signals necessa

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

23 isolated from the pancreatic infiltrates of nonobese diabetic mice have been shown to recognize epit

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

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

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

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

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

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

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

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

32 In nonobese diabetic mice with uncontrolled type 1 diabetes

33 NLPs ameliorated chronic progressive EAE in nonobese diabetic mice, a model which resembles some asp

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

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

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

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

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

39 we examined the role of IL-23 in diabetes in nonobese diabetic mice.

40 corticosterone were investigated using male nonobese diabetic mice.

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

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

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

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

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

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

47 oimmune diabetes developing spontaneously in nonobese diabetic mice.

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

49 The nonobese diabetic mouse model of human T1DM reveals that

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

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

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

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

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

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

56 ting cells during autoimmune diabetes in the nonobese diabetic mouse.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

77 Daily oral PAHSA administration to nonobese diabetic (NOD) mice delayed the onset of T1D an

78 Ins2-CCL21 transgenic, nonobese diabetic (NOD) mice express CCL21 in pancreatic

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

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

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

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

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

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

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

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

87 Nonobese diabetic (NOD) mice provide an excellent model

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

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

90 Nonobese diabetic (NOD) mice spontaneously develop type

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

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

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

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

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

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

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

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

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

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

101 In nonobese diabetic (NOD) mice, a model of T1D, diabetes d

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

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

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

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

106 6-67 of I-Abeta(g7) (I-A(b-g7)) in wild-type nonobese diabetic (NOD) mice, as well as NOD mice coexpr

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

132 ion decreased with age in autoimmunity-prone nonobese diabetic (NOD) mice.

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

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

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

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

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

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

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

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

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

142 engraftment and therapeutic efficacy in the nonobese diabetic (NOD) mouse model of autoimmune diabet

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

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

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

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

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

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

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

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

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

152 Leveraging the diabetes-susceptible nonobese diabetic (NOD) mouse model, we phenocopy the di

153 1 diabetes (T1D) susceptibility locus in the nonobese diabetic (NOD) mouse model.

154 facilitated by preclinical studies using the nonobese diabetic (NOD) mouse model.

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

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

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

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

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

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

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

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

163 1 diabetic patients and an animal model, the nonobese diabetic (NOD) mouse, show morphological and fu

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

197 Nonobese diabetic RIP-IL35 transgenic mice exhibited dec

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

199 HCC cells with AATF stably knocked down into nonobese diabetic scid gamma mice demonstrated reduced t

200 val in C4-2 or C4-2 TP53 (-/-) tumor-bearing nonobese diabetic scid gamma-mice.

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

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

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

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

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

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

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

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

209 34(+) fetal liver cells into immunodeficient nonobese diabetic severe combined immunodeficiency (NOD/

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

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

212 Further, the nonobese diabetic severe combined immunodeficiency commo

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

214 Six nonobese diabetic severe combined immunodeficiency mice

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

216 Humanized nonobese diabetic severe combined immunodeficient common

217 Nonobese diabetic severe combined immunodeficient gammac

218 In contrast to nonobese diabetic severe combined immunodeficient Il2rg(

219 Nonobese diabetic severe combined immunodeficient mice l

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

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

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

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

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

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

226 as assessed by transplantation into diabetic nonobese diabetic-severe combined immunodeficiency mouse

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

228 Nonobese diabetic-severe combined immunodeficiency-gamma

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

247 Nonobese diabetic/severe combined immunodeficiency (NOD/

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

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

250 Nonobese diabetic/severe combined immunodeficiency mice

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

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

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

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

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

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

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

258 Using a nonobese diabetic/severe combined immunodeficiency mouse

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

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

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

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

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

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

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

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

267 ribution and SPECT imaging were done on male nonobese diabetic/severe combined immunodeficient (NOD/S

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

287 In nonobese diabetic/severe combined immunodeficient mice b

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

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

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

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

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

293 gh CXCR4/CXCL12 signals as shown in chimeric 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.