ライフサイエンスコーパス: NOD mouse

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

2 pecific model and the spontaneously diabetic NOD mouse.

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

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

5 regulator of diabetes susceptibility in the NOD mouse.

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

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

8 utoimmune diseases including diabetes in the NOD mouse.

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

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

11 incorporates a strong immune phenotype: the NOD mouse.

12 mically induced diabetes pathogenesis in the NOD mouse.

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

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

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

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

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

18 munity and destructive autoreactivity in the NOD mouse.

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

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

21 ed in the etiology of type 1 diabetes in the NOD mouse.

22 t macrophages as insulitis progresses in the NOD mouse.

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

24 of autoimmune diabetes in the unmanipulated NOD mouse.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

53 NOD mouse AIP was associated with severe periductal and

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

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

56 study, we examined the role of NOX2 in both NOD mouse and human CD8+ T cell function.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

76 n both human T1D and the non-obese diabetic (NOD) mouse, but whether these impairments reflect intrin

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

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

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

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

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

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

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

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

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

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

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

88 The NOD mouse develops spontaneous type 1 diabetes, with som

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

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

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

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

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

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

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

96 ) genes, and protects the nonobese diabetic (NOD) mouse from T1D.

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

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

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

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

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

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

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

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

105 A vaccine tailored to the nonobese diabetic (NOD) mouse in parallel to one expressing the Proinsulin

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

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

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

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

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

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

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

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

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

115 The NOD mouse is genetically predisposed to the development

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

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

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

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

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

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

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

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

124 e found that human type 1 diabetes (T1D) and NOD mouse islets show reduced B-cell STX4 expression, co

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

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

127 to T1D-associated cytokines and in diabetic NOD mouse islets.

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

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

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

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

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

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

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

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

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

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

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

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

140 he progression of autoimmune diabetes in the NOD mouse model and is characterized by defects in Treg

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

175 The NOD mouse model recapitulates multiple features of human

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

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

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

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

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

181 In humans with type 1 diabetes (T1D) and the NOD mouse model, a T cell-mediated autoimmune destructio

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

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

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

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

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

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

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

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

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

191 islet allograft survival in the challenging NOD mouse model.

192 tes type 1 diabetes (T1D) development in the NOD mouse model.

193 for type 1 diabetes (T1D) development in the NOD mouse model.

194 1Ver) accelerated autoimmune diabetes in the NOD mouse model.

195 antigen for diabetogenic CD4+ T cells in the NOD mouse model.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

222 y of euglycemia in a T1D, nonobese diabetic (NOD) mouse model, by suppressing glucagon secretion.

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

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

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

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

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

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

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

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

231 hyperglycemia in Lnglc human CD20 transgenic NOD mouse models.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

252 The NOD mouse spontaneously develops autoimmune diabetes and

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

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

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

256 The NOD mouse strain spontaneously develops autoimmune diabe

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

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

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

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

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

262 mortality than observed in previous HLA-DQ8 NOD mouse strains.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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