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 receiving transient BAFF blockade were characte

3 NOD mice transgenically expressing Ig molecules recogniz

4 NOD mice treated with AZD1480 were protected from autoim

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

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

7 NOD treatment significantly reduced neointima formation

8 NOD-Idd22 mice exhibit almost complete protection from s

9 NOD-like receptors (NLRs) are central components of the

10 NOD-Scid-IL2Rgamma null mice were transplanted with huma

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

12 and female SjS-susceptible (SjS(s)) C57BL/6.NOD-Aec1Aec2 mice.

13 by genetically ablating Il-17 in the C57BL/6.NOD-Aec1Aec2, spontaneous SjS murine model.

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

15 Using ICG-001 in a NOD/SCID/IL2Rgamma(-/-) mouse model of engrafted human c

16 tute the radiation-depleted bone marrow of a NOD/SCID/IL2rg(-/-) (NSG) mouse on which a patient's tum

17 method of intrahepatic injection into adult NOD.Cg-Prkdc(scid)Il2rg(tm1Wjl)/SzJ mice liver of both a

18 lyze the therapeutic effects of sGARP, adult NOD/Scidgammac(-/-) (NSG) mice received peripheral blood

19 As these data suggest that also NOD might be cleared fast, further pharmacokinetic evalu

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

21 linked genetic variants between the B10 and NOD genome are required for the diabetes protection conf

22 1 IFN and express higher levels of CD40, and NOD monocyte DCs make more TNF.

23 uggest that modulation of the expression and NOD activity of Cygb represents a strategy for the treat

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

25 s from SHP-1-deficient (Shp-1(-/-)) mice and NOD.NOR-Idd13.Prkdc(scid) (NS-Idd13) mice, as well as hu

26 d proliferated to the same extent in NOD and NOD-Idd22 mice, yet the accumulation of pathogenic CTLs

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

28 sly develops pathogenic TSHR autoantibodies, NOD.H2(h4) mice with the human (h) TSHR (hTSHR) A-subuni

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

30 cantly increased the survival of PEL bearing NOD-SCID mice in an orthotopic xenograft model as compar

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

32 roducts in the cytosol of mammalian cells by NOD-like receptors leads to the activation of caspase-1

33 sensed and restricted in vivo, especially by NOD-like receptor (NLR) inflammasomes, is largely unknow

34 aved caspase-3) was significantly reduced by NOD.

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

36 diabetogenic virus, Coxsackievirus B3 (CB3), NOD.Ncf1(m1J) mice remained resistant to virus-induced a

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

38 Thus, we generated and characterized NOD mice transgenically expressing an Ig molecule repres

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

40 In conclusion, NOD DCs display altered innate responses characterized b

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

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

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

44 In immune-deficient NOD/Shi-scid, gammacnull (NSG) mice, administration of C

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

46 4(+) and CD8(+) T cells from c-Rel-deficient NOD mice showed significantly decreased T-cell receptor-

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

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

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

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

51 vage of vehicle (dH2O) in nonobese diabetic (NOD) mice induced a social avoidance behavior that was n

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

53 f a miRNA92a antagomir to nonobese diabetic (NOD) mice with ongoing islet autoimmunity resulted in a

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

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

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

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

58 By using non-obese diabetic (NOD) BDC2.5 TCR-transgenic (Tg), and IL-10 and Foxp3 dou

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

60 1 diabetes in humans and non-obese diabetic (NOD) mice.

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

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

63 ised mice [BALB scid and non-obese diabetic (NOD) scid strains] causing lethal infection without prio

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

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

66 and diabetes was reversed in newly diagnosed NOD mice.

67 ication systems are Hmp, an NO. dioxygenase (NOD), and NorV, an NO. reductase (NOR).

68 ty related to both nitric oxide dioxygenase (NOD) and nitrite reductase (NiR) activity.

69 catalytic cycle of nitric oxide dioxygenase (NOD) enzymes, which facilitate a .NO homeostatic process

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

71 f nucleotide-binding oligomerization domain (NOD) 1 and NOD2 by muropeptides triggers a complex trans

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

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

74 Nucleotide-binding oligomerization domain (NOD)-like receptor family, pyrin domain-containing prote

75 e nucleotide-binding oligomerization domain (NOD)-like receptor protein 3 (NLRP3) inflammasome to rec

76 n nucleotide binding oligomerization domain (NOD)-like receptors (NLRs), retinoic acid-inducible prot

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

78 TLRs, and nucleotide oligomerization domain (NOD)-like receptors.

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

80 Because N-octanoyl dopamine (NOD) inhibits vascular inflammation and suppresses T cel

81 ns of potential donors, N-octanoyl dopamine (NOD) treatment might be considered as it does not affect

82 Ealpha16/NOD females vertically protected their NOD offspring fro

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

84 thymocyte maturation defects, and exogenous NOD ligands can enhance thymocyte maturation in culture.

85 ofluorination of the NOD-derivative [(18)F]F-NOD [(18)F]5 for in vivo assessment of NOD's elimination

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

87 of a blocking antibody to 6 week-old female NOD/ShiLtJ mice repeatedly during a 9-day period.

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

89 the IFN-alpha/beta receptor because DCs from NOD and B6 mice show similar CpG-induced CD86 levels whe

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

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

92 Sixty to seventy percent of IFN-gamma(-/-) NOD.H-2h4 mice given sodium iodide (NaI)-supplemented wa

93 ae and Ruminococcaceae, from vehicle-gavaged NOD donors to microbiota-depleted C57BL/6 recipients was

94 However, NOD-Idd22 mice were highly protected against adoptive tr

95 s and miR-375 of human islets in a humanized NOD scid gamma (NSG) mouse model, whose immune reaction

96 ure a P. falciparum infection in a humanized NOD/SCID mouse model system.

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

98 nted viral rebound in HIV-infected humanized NOD scid IL-2Rgamma(-/-) bone marrow-liver-thymus mice u

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

100 This study identified NOD as potential treatment modality to attenuate TV.

101 ist A438079 in the CD28(-/-), IFNgamma(-/-), NOD.H-2(h4) mouse model of salivary gland exocrinopathy

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

103 e diabetic/severe combined immunodeficiency (NOD/SCID) mice with partially reconstituted immune syste

104 Immunodeficient NOD.Cg-Prkdc(scid)IL2rg(tm1Wjl)(NSG) mice were reconstit

105 mor burden in BLCL-engrafted immunodeficient NOD-SCID/Il2rg(-/-) mice.

106 cell activation factor into immunodeficient NOD scid gamma (NSG) mice by the use of an adeno-associa

107 ing and transplantation into immunodeficient NOD/SCID/interleukin 2 receptor gamma chain null mice.

108 L/6, BALB/c, or the severely immunodeficient NOD-scid,gammac(null) [NSG]).

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

110 In NOD mice depleted of islet-resident macrophages starting

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

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

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

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

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

116 Runx2 knockdown invasive MDA-MB-231 cells in NOD/SCID mice, and compared parental and bone-derived va

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

118 In contrast, in NOD.ChgA(+/+) mice, a majority of the ChgA-reactive T ce

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

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

121 d also strongly inhibited T1D development in NOD mice.

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

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

124 on and development of autoimmune diabetes in NOD mice.

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

126 ing early-onset autoimmune diabetogenesis in NOD mice.

127 experimental autoimmune thyroiditis (EAT) in NOD mice expressing human DRbeta1-Arg74.

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

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

130 node and proliferated to the same extent in NOD and NOD-Idd22 mice, yet the accumulation of pathogen

131 Also found in NOD islets is a minor population of dendritic cells (DCs

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

133 ation and preserves secretory functioning in NOD/ShiLtJ SS-like mice.

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

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

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

137 ccurring islet-infiltrating B-lymphocytes in NOD mice recognizing the neuronal antigen peripherin.

138 induced transcriptional response is muted in NOD cDCs.

139 This was not observed in NOD animals with depleted microbiota via oral administra

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

141 teraction significantly delayed T1D onset in NOD mice.

142 peripheral blood mononuclear cells (PBMC) in NOD/SCID mice harboring xenografts of MDA-MB-231, a trip

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

144 ed a significant delay in AML progression in NOD/SCID/IL2Rg(null) mice, but the persistence of adopti

145 rwent vigorous intrasplenic proliferation in NOD.IFN-gamma(null) recipients.

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

147 on of activated STAT1 is markedly reduced in NOD CD11c(+) cells, consistent with lower type 1 IFN res

148 s in the islets was significantly reduced in NOD-Idd22 mice, correlating with disease resistance.

149 slet-infiltrating CD8 T cells was reduced in NOD.Tnfrsf9(-/-) mice in part because of their decreased

150 The impaired response in NOD DCs is likely downstream of the IFN-alpha/beta recep

151 promising approach for diabetes reversal in NOD mice.

152 to impaired proinflammatory TLR signaling in NOD.Ncf1(m1J) macrophages.

153 1 hinders the development and onset of SS in NOD mice, in part by suppressing IFN-gamma production.

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

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

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

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

158 LT3.Fc inhibited progression of human TCL in NOD.Cg-Prkdc Il-2rg/SzJ mice, suggesting its potential i

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

160 rden of mutant IDH1 AML cells xenografted in NOD-Scid-IL2rgamma(null)mice and markedly increased over

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

162 e of Streptococcus correlated with increased NOD-like receptor signaling.

163 We hypothesized that Gal3 is a key to induce NOD-like receptor family, pyrin domain containing 3 (NLR

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

165 hei-infected mice and P. falciparum-infected NOD-scid IL-2Rgamma(null) mice.

166 topoietic stem cell engrafted virus-infected NOD.Cg-Prkdc(scid) Il2rg(tm1Wjl)/SzJ mice.

167 Interestingly, NOD Rag1(-/-) mice also display a defect in CpG-induced

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

169 and a homology-directed repair template into NOD single-cell zygotes to introduce the Ptpn22(R619W) m

170 ivo in the PLNs after adoptive transfer into NOD recipients.

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

172 eplication in human islets transplanted into NOD-scid IL-2Rg(null) mice.

173 1 and NOD2, two members of the intracellular NOD-like receptor family, sense bacterial peptidoglycan-

174 s) were injected into sublethally-irradiated NOD-scid-IL2Rg-/- (NSI) mice.

175 T1D pathogenesis, as NOX-deficient NOD mice (NOD.Ncf1(m1J) ) were protected against T1D due, in part,

176 espread use of nonobese diabetic (NOD) mice, NOD with severe combined immunodeficiency (scid) mutatio

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

178 em (T3SS) needle complex that induces NLRC4 (NOD-like receptor C4) activation, interleukin-1beta (IL-

179 nt Domain (CARD)), pro-caspase-1, and NLRP3 (NOD-Like Receptor family Pyrin domain containing 3).

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

181 s of the large family of intracellular NLRs (NOD-like receptors), which also includes animal immune r

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

183 As controls, nontransgenic NOD.H2(h4) mice similarly injected with inactive hTSHR A

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

185 mbryonic stem (ES) cells to generate a novel NOD transgenic line with the 77A/G SNP.

186 Herein we show that NRG (NOD.RagKO.IL2RgammacKO) mice expressing HLA-DR4 molecule

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

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

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

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

191 8)F]F-NOD [(18)F]5 for in vivo assessment of NOD's elimination kinetics by means of PET imaging.

192 n islets grafted under the kidney capsule of NOD-scid IL2Rg(null) mice.

193 pression is reduced in Valpha14iNKT cells of NOD mice.

194 learly support a vasculoprotective effect of NOD by reducing smooth muscle cell proliferation and inf

195 e cells were performed to test the effect of NOD on proliferation (WST-1 assay), cell cycle (flow cyt

196 eproduces the immunopathological features of NOD ABD.

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

198 metastatic nodule formation in the lungs of NOD/SCID mice.

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

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

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

202 on in Xrcc4 and Glis3 alters the response of NOD beta cells to unfolded protein stress, enhancing the

203 Although studies have addressed the role of NOD proteins in innate immune responses, little attentio

204 RNA sequencing of NOD.Abd3 common bile duct early in disease demonstrates

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

206 Treatment of NOD mice starting at 10 wk of age, when the autoimmune p

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

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

209 significantly associated with inhibition of NODs and TLRs, whereas increased abundance of Streptococ

210 T cell homeostasis, are upregulated less on NOD cDCs.

211 tion of human RDEB skin xenografts placed on NOD-scid IL2Rgamma(null) recipients, with reconstruction

212 eptor therapy reverses diabetes in new onset NOD mice.

213 To better assess optimal NOD concentrations for donor treatment, we report on the

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

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

216 In particular, NOD/SCID/IL2rg(-/-) mice can support the growth of vario

217 c-Rel-competent Treg cells from prediabetic NOD mice reversed the accelerated diabetes development i

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

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

220 tely on inhibition of the IL-1beta-producing NOD-like receptor family pyrin domain containing 3 infla

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

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

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

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

225 g oligomerization domain-containing protein (NOD) 2.

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

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

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

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

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

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

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

233 studies with BALB/c Rag2(-/-)Il2rg(-/-)Sirpa(NOD)Alb-uPA(tg/tg) mice, stably engrafted with human hep

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

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

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

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

238 nt thinking, an early intervention targeting NOD-like receptor family, pyrin domain containing 3 infl

239 We report in this article that NOD.ChgA(-/-) mice do not develop diabetes and show litt

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

241 in vitro, we here tested the hypothesis that NOD treatment ameliorates TV.

242 Surprisingly, the findings indicate that NOD mice lacking the HR (13R(-/-)) display resistance to

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

244 We previously reported that NOD.c3c4 mice develop spontaneous autoimmune biliary dis

245 In this study, we show that NOD.Tnfrsf9(-/-) CD8 T cells had significantly reduced d

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

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

248 The NOD-like receptor family members and the NALP3 inflammas

249 flow, and local tissue hypoxia activate the NOD-like receptor family pyrin domain containing 3 infla

250 tidylarginine deiminase 4, and activates the NOD-like receptor family, pyrin domain-containing 3 infl

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

252 ing mutations within 41 genes comprising the NOD signaling pathway in pIBD patients.

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

254 For example, the NOD strain carries a high percentage and absolute number

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

256 learance during IAV infection.IMPORTANCE The NOD-like receptor family member NLRC5 is known to regula

257 abrogating the sex bias normally seen in the NOD model.

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

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

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

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

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

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

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

265 the fast and facile radiofluorination of the NOD-derivative [(18)F]F-NOD [(18)F]5 for in vivo assessm

266 NLRC4 and NLRP3, of the NOD-like receptor (NLR) family of intracellular proteins

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

268 NLRC5, a member of the NOD-like receptor (NLR) protein family, has recently bee

269 show that NOD1 and NOD2, two members of the NOD-like receptor family of PRRs, are important mediator

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

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

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

273 nstrate that knock-in transgenic mice on the NOD background can test causative mutations relevant in

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

275 This model is based on the NOD-scid IL2rg(null)SCF/GM-CSF/IL3 (NSG-SGM3) strain of

276 incorporates a strong immune phenotype: the NOD mouse.

277 to the C57BL/6 genetic background; thus, the NOD genetic background (which promotes autoimmunity) is

278 could also bind via its small subunit to the NOD domain in Apaf-1, resulting in the formation of a he

279 ne orthologous Ptpn22(R619W) mutation to the NOD genome would enhance the spontaneous development of

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

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

282 rotein lost the ability to interact with the NOD domain of NLRP3.

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

284 pha16/NOD females vertically protected their NOD offspring from diabetes and insulitis, an effect tha

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

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

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

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

289 aquaporin 5 expression in anti-PD-L1-treated NOD/ShiLtJ mice.

290 ansferred disease to otherwise unmanipulated NOD.IFN-gamma(null) , but not standard NOD, mice.

291 To investigate this link, we have used NOD embryonic stem (ES) cells to generate a novel NOD tr

292 Using NOD congenic mice, we validate that both the MHC and the

293 positive T cells in HIV-infected brain using NOD/SCID/IL-2rcgamma(-/-) mice reconstituted with human

294 ed suppression of insulitis was tested using NOD.Foxp3(DTR) mice, which show extensive islet infiltra

295 Among various NOD like receptors, NOD2 was significantly upregulated i

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

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

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

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

300 nic and rapidly transfer diabetes into young NOD recipients.