ライフサイエンスコーパス: NOD

1 NOD HSCs were held in their niche by excess expression o

2 NOD mice develop spontaneous autoimmune type 1 diabetes

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

4 NOD mice receiving Seriola dumerili transgenic islet tra

5 NOD mice treated with AZD1480 were protected from autoim

6 NOD scid gamma-(NSG) mice were inoculated with subcutane

7 NOD Scid IL-2Rgamma(-/-) (NSG) mice that had undergone p

8 NOD-Idd22 mice exhibit almost complete protection from s

9 NOD-like family pyrin domain containing 6 (NLRP6) is one

10 NOD-like receptor (NLR) family CARD domain containing 3

11 NOD-like receptors (NLR) are critical regulators of inna

12 NOD-like receptors (NLRs) localize in the cytosol to rec

13 NOD-like receptors play a role in regulation of innate i

14 NOD-PerIg mice are a previously developed BCR-transgenic

15 NOD-PerIg mice have accelerated T1D development, and Per

16 NOD-scidIL-2Rg(-/-) mice were given injections of LS174T

17 NOD.Cg-Prkdc(scid)Il2rg(tm1Wjl)/SzJ (NSG) mice were give

18 NOD.H2(h4) These findings emphasize the need for suffici

19 NOD/SCIDIL2RgammaNull-3/GM/SF mice transplanted with ARC

20 blockade induced a programmed death ligand 1/NOD-, LRR-, and pyrin domain-containing protein 3 (PD-L1

21 To address this, we created 2 NOD- scid IL-2 receptor subunit gamma ( IL2rg) (null) (N

22 We then treated 58 NOD.H-2(h4) mice for 12 wk with either unsupplemented wa

23 ll clone BDC-2.5, originally isolated from a NOD mouse, has been widely used to study the contributio

24 were only observed in xenografts grown in a NOD/SCID IL2 receptor gamma (NOG) knockout mouse strain

25 SF, interleukin-3, and stem cell factor in a NOD/SCID-IL2Rgamma(null) background (NSGS mice), we demo

26 RM, EC313, for the treatment for UFs using a NOD-SCID mouse model.

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

28 rotein (GFP) reporter, into irradiated adult NOD.Cg-Prkdc(scid) Il2rg(tm1Wjl) /SzJ (NSG) mice.

29 mice lacking IgM antibodies (Rag 2(-/-) and NOD-scid-gamma [NSG]).

30 MM1.7 melanoma cells in both C57BL/6Ncrl and NOD-scid IL2Rgamma(null) (NSG) mice.

31 rated that the allelic difference in B10 and NOD Tnfrsf9 alone was sufficient to cause differential a

32 cted intravenously into immune-competent and NOD/SCID mice, and lung metastases were quantified.

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

34 alcium in mediating thapsigargin-induced and NOD-dependent pro-inflammatory signaling, in part throug

35 A/J and NOD segments of genes in this region drove elevated HER2

36 udy, we explored how NAD(+) affects TLR4 and NOD-like receptor with a PYD-domain 3 (NLRP3) inflammaso

37 cemic (prediabetic) female NOD TLR4(+/+) and NOD TLR4(-/-) mice, gut morphology and microbiome compos

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

39 llular pattern recognition receptors such as NOD-like receptors have been minimally studied.

40 osolic pattern recognition receptors such as NOD-like receptors, NLRP3 inflammasomes.

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

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

43 in four inbred mouse strains: C57Bl/6J (B6), NOD/LtJ (NOD), 129S1/SvlmJ (S1), and A/J (AJ).

44 GSI treatment of MM tumor-bearing NOD/SCID/gammac-/- mice increased BCMA expression on tum

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

46 n response to canonical stimuli initiated by NOD-like receptor (NLR), and apoptosis-associated speck-

47 er report that these effects are mediated by NOD-like receptor family, pyrin domain containing 3 (NLR

48 ins of plants (R-proteins) and the so-called NOD-like receptors of animals (NLRs) share a domain arch

49 Both plants and animals carry NOD-like-receptors (NLRs).

50 CNR13/NOD is localized to the membrane and is enriched in divi

51 In contrast, NOD.Tnfrsf9(-/-) CD4 T cells highly promoted T1D develop

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

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

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

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

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

57 ice using the CRISPR/Cas9 system (designated NOD.Tnfsf9 (-/-)).

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

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

60 re-establish glucose homeostasis in diabetic NOD/SCID mice.

61 developed in streptozotocin-induced diabetic NOD/SCID mice.

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

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

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

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

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

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

68 erapeutic efficacy in the nonobese diabetic (NOD) mouse model of autoimmune diabetes using nonablativ

69 the diabetes-susceptible nonobese diabetic (NOD) mouse model, we phenocopy the diabetes progression

70 sceptibility locus in the nonobese diabetic (NOD) mouse model.

71 linical studies using the nonobese diabetic (NOD) mouse model.

72 Using nonobese diabetic (NOD)-scid IL2Rgammanull (NSG) mice reconstituted with a

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

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

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

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

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

78 The Non-obese Diabetic (NOD) mouse model for type I diabetes also develops some

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

80 Using a non-obese diabetic (NOD) mouse model, we have characterized changes in both

81 with T1D and mice of the non-obese diabetic (NOD) strain, we detected alterations in MAIT cells, incl

82 f Langerhans of 3-wk-old non-obese diabetic (NOD), NOD.Rag1(-/-), and B6.g7 mice.

83 t when transplanted into non-obese diabetic (NOD)-SCID-gamma (NSG) mice with detectable levels of gen

84 on in salivary glands in non-obese diabetic (NOD)/ShiLtJ, a mouse model for Sjogren's syndrome (SS).

85 and diabetes was reversed in newly diagnosed NOD mice.

86 ty of the specific nitric oxide dioxygenase (NOD) that serves as the main in vivo regulator of O2-dep

87 h nucleotide-binding oligomerization domain (NOD) 1 and/or NOD2 receptors.

88 e nucleotide-binding oligomerization domain (NOD) proteins could detect endoplasmic reticulum (ER) st

89 g nucleotide-binding oligomerization domain (NOD)-, Toll-, and RIG1-like receptor pathways, was assoc

90 d nucleotide-binding oligomerization domain (NOD)-like receptor C4 (NLRC4) were associated with neutr

91 f nucleotide-binding oligomerization domain (NOD)-like receptors and DEAD-box or DEAH-box RNA helicas

92 e nucleotide-binding oligomerization domain (NOD)-like receptors belong to the family of pattern reco

93 cleotide-binding and oligomerization domain (NOD)-like receptors NOD1 and NOD2 are cytosolic innate i

94 cleotide binding and oligomerization domain (NOD)-like receptors that were found to control nonself r

95 nucleotide-binding oligomerization domains (NODs) can also recognize a broader array of danger signa

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

97 n immune system mice were made by engrafting NOD/SCID/IL2Rgammanull (NSG) mice with human hematopoiet

98 d into in vivo efficacy in the P. falciparum NOD-scid IL-2Rgamma(null) (NSG) mouse model.

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

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

101 ks of age) compared to un-manipulated female NOD (diabetes onset at 12 weeks of age) and those receiv

102 er the kidney capsules of 5 weeks old female NOD wildtype mice.

103 0-day-old normoglycemic (prediabetic) female NOD TLR4(+/+) and NOD TLR4(-/-) mice, gut morphology and

104 d by a RIP2 inhibitor, suggesting a role for NOD signaling.

105 Pancreatic endothelial cells from NOD-Idd22 animals expressed lower levels of adhesion mol

106 re broadly elevated in plasma collected from NOD/ShiLtJ female mice after disease onset, whereas thes

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

108 (-/-) (NSIN) mice by knocking out Foxn1 from NOD/SCID/IL2rg(-/-) (NSI) mice using the CRISPR/Cas9 sys

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

110 e began in vitro using T cells isolated from NOD.H-2(h4) spleens and found that MYMD-1 suppressed TNF

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

112 e altered in submandibular glands (SMG) from NOD/ShiLtJ female mice after disease onset, with 5-LOX a

113 ransferred T cells or whole splenocytes from NOD-PerIg mice expectedly induce T1D in NOD.scid recipie

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

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

116 planted human islets in the liver of healthy NOD/SCID mice.

117 Host NOD-like receptor family pyrin domain-containing 6 (NLRP

118 development of pathogenic TSHR Abs in hTSHR/NOD.

119 p. four times at weekly intervals into hTSHR/NOD.H2(h4) mice with the goal of blocking TSHR Ab develo

120 However, in the hTSHR/NOD.H2(h4) model, enhancement is specific for TSHR Abs,

121 HLA-DR4+ bone marrow chimeras, and humanized NOD-scid IL-2Rgammanull mice to demonstrate for the firs

122 s study, we established a diabetic humanized NOD-scidIL2Rgamma(null) (NSG) mouse model of T-cell-medi

123 lly new anti-HIV Abs, we exploited humanized NOD-scid IL2rgamma(null) mice systemically infected with

124 for early biodosimetry triage from humanized NOD-scid-gamma (Hu-NSG) mice and non-human primates (NHP

125 uman Skin and Immune System (hSIS)-humanized NOD-scid IL2Rgamma(null) (NSG) mouse and Sprague-Dawley-

126 -sulfonic-acid model of colitis in humanized NOD/scid/gamma mice.

127 icantly milder hemotoxicity in the humanized NOD/SCID mouse model engrafted with red blood cells from

128 and reverse diabetes in newly hyperglycemic NOD mice.

129 nsplanted into Fah(-/-)/Rag2(-/-)/Il2rg(-/-)/NOD (FRGN) mice to create mice with humanized livers.

130 e diabetic/severe combined immunodeficiency (NOD-SCID) mice resulted in the formation of microvessels

131 Here we utilized immunodeficient NOD-scid IL2rgamma(null) (NSG) mice that carried in vivo

132 se diabetic/severe combined immunodeficient (NOD/SCID) mice bearing human PSMA(+) PC3 PIP and PSMA(-)

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

134 In NOD mice depleted of islet-resident macrophages starting

135 In this article, we demonstrate that ABD in NOD.c3c4 and related NOD ABD strains is caused by a chro

136 tigated whether SPM production is altered in NOD/ShiLtJ using metabololipidomics and enzyme-linked im

137 h in 3D spheroid growth assays as well as in NOD scid gamma (NSG) mice.

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

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

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

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

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

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

144 ulation of RGS12-overexpressed OSCC cells in NOD scid mice showed a significant reduction in tumor fo

145 able to form a tumor with only 100 cells in NOD-SCID or immunocompetent mice.

146 rowth ability of AGS gastric cancer cells in NOD/SCID mice.

147 Likewise, in vivo chemotaxis in NOD-scid-Il2rg(-/-) mice was reduced in IL-4-stimulated

148 ance that leads to autoimmune cholangitis in NOD.Abd3 congenic mice.

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

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

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

152 treatment, prevents diabetes development in NOD mice.

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

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

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

156 gen specificities and autoimmune diabetes in NOD mice.

157 ls suppressed the development of diabetes in NOD severe combined immunodeficiency mice receiving diab

158 derived tumors and xenografts established in NOD-SCID or nude mice, low MCPIP1 levels correlated stro

159 ene (MLL)-rearranged ALL were established in NOD.Cg-Prkdc(scid) Il2rg(tm1Wjl)/SzJ (NSG) mice.

160 cates to high titers in human lung grafts in NOD-SCID/gamma mice, resulting in a robust inflammatory

161 gression and rapid onset of hyperglycemia in NOD mice.

162 and [(55)Co]Co-DOTATATE by PET/CT imaging in NOD-SCID mice bearing subcutaneous somatostatin receptor

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

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

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

166 at abnormal lymphocyte responses observed in NOD-dependent inflammatory diseases are not driven solel

167 ajor contributors to autoimmune pathology in NOD mice.

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

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

170 ng loci coalesced enhancers and promoters in NOD, but not C57BL/6 thymocytes.

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

172 promising approach for diabetes reversal in NOD mice.

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

174 responses and promote beta cell survival in NOD mice.

175 induces psoriatic arthritis-like symptoms in NOD mice.

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

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

178 from NOD-PerIg mice expectedly induce T1D in NOD.scid recipients but, depending on the kinetics of di

179 secretion and improved glucose tolerance in NOD mice.

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

181 icity assays as well as adoptive transfer in NOD/SCID/IL2Rgamma mice were used to assess for pathogen

182 showed significantly higher tumorigenesis in NOD/Scid/IL2Rgamma-null mice, and immunostaining of mous

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

184 in-interaction network, missense variants in NOD-like receptor family genes (NOD2, NLRC4, NLRP3, and

185 and mutant ER-expressing tumor xenografts in NOD/SCID-gamma mice after oral or subcutaneous administr

186 in NB4 cells decreased the tumor burden in (NOD scid gamma) NSG mice, suggesting its implication in

187 The calcium ionophore A23187 also induced NOD-dependent signaling, and calcium chelators demonstra

188 Here, we confirm that thapsigargin induces NOD-dependent pro-inflammatory signaling in epithelial c

189 xogenous superoxide addition to CB3-infected NOD.Ncf1(m1J) bone marrow-derived macrophages rescued th

190 c (expressing solely Seriola dumerili Ins2), NOD, or B16:A-dKO islets under the kidney capsules of 5

191 Interestingly, NOD/SCID mice, which have a deficiency in T, B, and NK c

192 Adoptive transfer of splenic T cells into NOD.Rag1(-/-) mice demonstrated that UBASH3A deficiency

193 ts of NOD mice and transferred diabetes into NOD/scid recipients.

194 Treg cells were adoptively transferred into NOD SCID gammaC-deficient mice, which were given isotype

195 nbred mouse strains: C57Bl/6J (B6), NOD/LtJ (NOD), 129S1/SvlmJ (S1), and A/J (AJ).

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

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

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

199 Whereas MHC-matched NOD-LNSC significantly reduced G9Calpha(-/-)CD8(+) T-cel

200 To examine these mechanisms, NOD/SCID IL-2 RG(-/-) humanized mice were either directl

201 In particular, S100A9-mediated NOD-like receptor protein 3 (NLRP3) inflammasome activat

202 dium were required for thapsigargin-mediated NOD activation.

203 nd ex vivo Compared with NOD TLR4(+/+) mice, NOD TLR4(-/-) animals showed lower muscle mass of the sm

204 DOMAIN CONTAINING RECEPTOR KINASE3 (MtLYK3)-NOD FACTOR PERCEPTION (MtNFP; M. truncatula).

205 The NODcALR-(D8Mit293-D8Mit137)/Mx (NOD-Idd22) recombinant congenic mouse strain was generat

206 if (LysM)-type transmembrane receptors named NOD FACTOR RECEPTOR1 (LjNFR1) and LjNFR5 (L. japonicus)

207 NLRP3 (NOD-, LRR- and pyrin domain-containing protein 3) is an

208 n endothelial cells that assembles an NLRP3 (NOD-like receptor pyrin domain-containing protein 3) inf

209 ultures, internalized MAC also causes NLRP3 (NOD-like receptor family pyrin domain containing 3) tran

210 recent evidence that the NOD2 target, NLRP3 (NOD-like receptor family, pyrin domain containing 3) is

211 ibility of specific inhibition of the NLRP3 (NOD-, LRR-, and pyrin domain-containing protein 3) infla

212 erhans of 3-wk-old non-obese diabetic (NOD), NOD.Rag1(-/-), and B6.g7 mice.

213 (ATX), cylindrospermopsin (CYN), nodularin (NOD), and microcystin-LR (MC-LR), in parallel, with the

214 ell autoantigens compared with nontransgenic NOD TLOs found in inflamed islets.

215 A novel NOD congenic mouse expressing aberrant Pkhd1, but lackin

216 t study, we generated a novel strain of nude NOD/SCID/IL2rg(-/-) (NSIN) mice by knocking out Foxn1 fr

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

218 n is significantly reduced in the absence of NOD proteins, but receptor-interacting protein 2 is not

219 d neuritis still developed in the absence of NOD-PerIg CD8(+) T cells but required CD4(+) T cells.

220 and orientation on the binding affinities of NOD-like receptors (NLRs).

221 jection of U2OS cells into the tibia bone of NOD-scid mice, which indicated that miR-449a and miR-424

222 eproduces the immunopathological features of NOD ABD.

223 erum suggests that a homeostatic function of NOD signaling may have been previously overlooked.

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

225 IRF5 signaling axis functions independent of NOD-like receptors and is critically required for the re

226 t-emitting diodes (LED) prior to infusion of NOD/SCID-IL2Rgamma(-/-) mice.

227 he inflammasome with a specific inhibitor of NOD-, LRR-, and pyrin domain-containing protein 3.

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

229 O. tsutsugamushi reduces cellular levels of NOD-, LRR-, and CARD-containing 5 (NLRC5), a recently id

230 Thus, our results suggest that a loss of NOD-LNSC MHC-independent suppressive mechanisms may cont

231 confirmed in the adoptive transfer model of NOD-SCID mice where tolDCs delayed diabetes onset.

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

233 e increasing Treg activation in pancreata of NOD mice.

234 depletion delayed T1D onset in a portion of NOD-PerIg mice, allowing them to survive long enough to

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

236 sis of 143B cells injected into the tibia of NOD SCID gamma mice.

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

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

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

240 ir of F1 hybrids expressed either the B10 or NOD Tnfrsf9 allele mimicking coisogenic strains.

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

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

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

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

245 Despite reduced IL-15 trans-presentation, NOD Ly-49(+) CD8 Tregs can effectively transduce IL-15-m

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

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

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

249 Furthermore, baicalein reduced NOD-like receptor 3 (NLRP3) inflammasome activation and

250 t lacking the c3 and c4 chromosomal regions (NOD.Abd3), reproduces the immunopathological features of

251 eroxide in the mechanisms tightly regulating NOD-like receptor family, pyrin domain containing 3 acti

252 demonstrate that ABD in NOD.c3c4 and related NOD ABD strains is caused by a chromosome 1 region that

253 Genomic and proteomic analyses revealed NOD and Ealpha16/NOD mice to host mild but significant d

254 NOD mice, which was enhanced by loss of SAP NOD T cells override SAP requirement to undergo activati

255 A soluble NOD-specific ligand and a soluble beta-glucan were used

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

257 (+) CD8 Treg development, we determined that NOD macrophages inadequately trans-present IL-15.

258 (HTLV-1(WT)) and HTLV-1(p12KO) We found that NOD/SCID/gamma(C) (-/-) c-kit(+) mice engrafted with hum

259 We propose that NOD coordinates cell activity in response to intrinsic a

260 Analysis of nod-1 sectors suggests that NOD plays a cell-autonomous function in the leaf.

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

262 ism(s) of the action of MYMD-1, we chose the NOD.H-2(h4) mouse model of spontaneous thyroiditis.

263 d variation in 40 of 41 genes comprising the NOD signaling pathway.

264 e for T1D, but the autoimmune process in the NOD model retains pathogenic Tfh without SAP.

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

266 n of islet-infiltrating B lymphocytes in the NOD mouse model of T1D produce Abs directed against the

267 CD70 signaling on disease progression in the NOD mouse model of type 1 diabetes (T1D).

268 gulate low-avidity autoreactive cells in the NOD mouse model of type 1 diabetes.

269 t macrophages as insulitis progresses in the NOD mouse.

270 ane potential of aging type I neurons in the NOD, ARHL model, was significantly hyperpolarized, and a

271 linked to gain-of-function mutations in the NOD-like receptor family, pyrin domain containing 3 (NLR

272 o wild-type NOD mice, T1D development in the NOD.Tnfsf9 (-/-) strain was significantly delayed, and m

273 Members of the NOD-like receptor (NLR) family of pathogen recognition r

274 s as well as expression of components of the NOD-like receptor family pyrin domain-containing protein

275 NOD2 is a member of the NOD-like receptor family that initiates inflammatory sig

276 NLRP12, a member of the NOD-like receptor family, is expressed in myeloid and bo

277 ata are pointing to an important role of the NOD-like receptor family, pyrin domain containing 3 (NLR

278 t transient, increase in the activity of the NOD-like receptor family, pyrin domain containing 3 infl

279 The key role of the NOD-like receptor family, pyrin domain containing 3 infl

280 results demonstrate the potential use of the NOD-scid IL2rgamma(null) mouse model to evaluate vaccine

281 e explored the suitability of the use of the NOD-scid IL2rgamma(null) mouse to study osteoarticular b

282 propose that loss of functional Pkhd1 on the NOD background produces early bile duct abnormalities, i

283 ment of a humanized mouse model based on the NOD-scid IL2rg(null) (NSG) mouse to study CRS in vivo.

284 We revisited this hypothesis using the NOD murine model of type 1 diabetes.

285 on the AML xenograft model in mice using the NOD/LtSz-scid IL2Rgammac null (NSG) mice.

286 orphisms (SNP) of toll-like receptors (TLR), NOD-like receptors (NLR) and RIG-I-like receptors (RLR)

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

288 n resulted in weaker adherence of T cells to NOD-Idd22 endothelium compared with NOD-derived endothel

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

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

291 Transgenic NOD.H2(h4) mice that express the human (h) TSHR A-subuni

292 T-cell receptor (TCR) alpha-chain transgenic NOD mouse on a TCRCalpha and proinsulin 2 (PI2)-deficien

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

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

295 echocardiography was used to assess whether NOD.Cg-Prkdc(scid) Il2rgt(m1Wjl)/SzJ mice reconstituted

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

297 e measured in vivo and ex vivo Compared with NOD TLR4(+/+) mice, NOD TLR4(-/-) animals showed lower m

298 cells to NOD-Idd22 endothelium compared with NOD-derived endothelium.

299 med a linkage analysis on F2 (B6.Rag1(-/-) x NOD.Rag1(-/-) intercross) mice.

300 ung cancer tumor growth in a mouse xenograft NOD-SCIDgamma model.