ライフサイエンスコーパス: autoimmune diabetes

1 nzyme A deficiency in the NOD mouse model of autoimmune diabetes.

2 ion treatment of NOD mice effectively treats autoimmune diabetes.

3 IGRP(206-214)) during the earliest stages of autoimmune diabetes.

4 ing this strain with NOD develop spontaneous autoimmune diabetes.

5 eage, which is destroyed in individuals with autoimmune diabetes.

6 G6pc2 is not essential for the emergence of autoimmune diabetes.

7 f the islets of Langerhans and their role in autoimmune diabetes.

8 pancreas and contributed to protection from autoimmune diabetes.

9 ted the onset of disease in a mouse model of autoimmune diabetes.

10 ne was not sufficient to prevent spontaneous autoimmune diabetes.

11 as to ascertain the role of complement C3 in autoimmune diabetes.

12 ord blood transfusion to treat patients with autoimmune diabetes.

13 p3(+) cells in the BCD2.5/NOD mouse model of autoimmune diabetes.

14 1J) mice remained resistant to virus-induced autoimmune diabetes.

15 cytokines, does not reduce the incidence of autoimmune diabetes.

16 genic upon adoptive transfer in the model of autoimmune diabetes.

17 lity, enhanced T cell-DC contacts and caused autoimmune diabetes.

18 bout 2% of LEW.1WR1 rats develop spontaneous autoimmune diabetes.

19 cell tolerance, and prevent T cell-mediated autoimmune diabetes.

20 les in allograft rejection and recurrence of autoimmune diabetes.

21 and reprogram B-cells to effectively reverse autoimmune diabetes.

22 ive RIP-OVA mice is also sufficient to cause autoimmune diabetes.

23 t for development of novel therapies to cure autoimmune diabetes.

24 d effective means to treat disorders such as autoimmune diabetes.

25 that has to be placed in the perspective of autoimmune diabetes.

26 tope and T-cell autoreactivity in a model of autoimmune diabetes.

27 eactive T cells that promotes development of autoimmune diabetes.

28 utoreactivity for the PI-1(47-64) epitope in autoimmune diabetes.

29 vo BLyS neutralization for the prevention of autoimmune diabetes.

30 iated inflammation using a transfer model of autoimmune diabetes.

31 OD strain of mice that spontaneously develop autoimmune diabetes.

32 ouse is an invaluable model for the study of autoimmune diabetes.

33 strategy for immunotherapy in patients with autoimmune diabetes.

34 al value of rituximab as a novel therapy for autoimmune diabetes.

35 ys nonredundant roles in the pathogenesis of autoimmune diabetes.

36 (NOD) mouse, a spontaneous, chronic model of autoimmune diabetes.

37 CD25- also participates in the regulation of autoimmune diabetes.

38 y T cells, and the animals rapidly developed autoimmune diabetes.

39 o local inflammation, islet destruction, and autoimmune diabetes.

40 fer suppressor function in a murine model of autoimmune diabetes.

41 ransplantation in humans and is effective in autoimmune diabetes.

42 agonist protected NOD mice from spontaneous autoimmune diabetes.

43 iabetic (NOD) mice, an experimental model of autoimmune diabetes.

44 with autoantigens might alter the course of autoimmune diabetes.

45 e of c-Rel in the development of spontaneous autoimmune diabetes.

46 lin may indeed be the target antigen causing autoimmune diabetes.

47 in-induced diabetes, a drug-induced model of autoimmune diabetes.

48 represents a mechanism of protection against autoimmune diabetes.

49 icient than polyclonal T(reg) in suppressing autoimmune diabetes.

50 , respectively, is completely protected from autoimmune diabetes.

51 cells that will attack beta cells leading to autoimmune diabetes.

52 the relationship between viral infection and autoimmune diabetes.

53 K(b)/A12-21-monospecific CD8(+) T cells and autoimmune diabetes.

54 play an important pathophysiological role in autoimmune diabetes.

55 e previously been implicated as a trigger of autoimmune diabetes.

56 ice spontaneously developed T cell-dependent autoimmune diabetes.

57 D (GAD65), serve as determinants of risk for autoimmune diabetes.

58 lished NOD and transgenic RIP-LCMV models of autoimmune diabetes.

59 on beta cells accelerates the development of autoimmune diabetes.

60 IL-21, is a key factor in susceptibility to autoimmune diabetes.

61 nst multiple low-dose streptozotocin-induced autoimmune diabetes.

62 s and may be important for the initiation of autoimmune diabetes.

63 of multiple low-dose streptozotocin-induced autoimmune diabetes.

64 sponses, prompting us to examine its role in autoimmune diabetes.

65 ia that is associated with the expression of autoimmune diabetes.

66 e role of this pathway in the development of autoimmune diabetes.

67 e in the progeny, influencing development of autoimmune diabetes.

68 ce defect is higher than that for preventing autoimmune diabetes.

69 or TRAIL deficiency in two animal models of autoimmune diabetes.

70 n in BBDR rats and permits the expression of autoimmune diabetes.

71 to block the JAK-STAT pathway would prevent autoimmune diabetes.

72 o enhanced susceptibility to virus-triggered autoimmune diabetes.

73 that HA is critical for the pathogenesis of autoimmune diabetes.

74 yte deletion, BIM, in the NOD mouse model of autoimmune diabetes.

75 Th17 cells contributes to the development of autoimmune diabetes.

76 The NOD mouse strain spontaneously develops autoimmune diabetes.

77 which to study the development and onset of autoimmune diabetes.

78 er may be sufficient to confer resistance to autoimmune diabetes.

79 the highest risk of developing experimental autoimmune diabetes.

80 ancreatic islets and a slower progression to autoimmune diabetes.

81 1D and is dispensable for the development of autoimmune diabetes.

82 the therapeutic potential of these cells in autoimmune diabetes.

83 ansactivator Tbx21/Tbet, and amelioration of autoimmune diabetes.

84 tolerance, allowing reversal of established autoimmune diabetes.

85 driving disease progress in animal models of autoimmune diabetes.

86 play a critical role in the pathogenesis of autoimmune diabetes.

87 marily characterized, in the pathogenesis of autoimmune diabetes.

88 e of Tregs and autoreactive cells regulating autoimmune diabetes.

89 ted the potential of this subset to initiate autoimmune diabetes.

90 least in large part, in the pathogenesis of autoimmune diabetes.

91 nhanced susceptibility to the development of autoimmune diabetes.

92 the peripheral blood of humans with type 1 (autoimmune) diabetes.

93 Among 182 F2 rats, 57 (31%) developed autoimmune diabetes after a mean latency of 16 days.

94 s I molecule is required to induce recurrent autoimmune diabetes after pancreas transplantation in mi

95 Inflammatory cytokines are involved in autoimmune diabetes: among the most prominent is interle

96 uppressed immunopathology in mouse models of autoimmune diabetes and airway inflammation, and increas

97 ve identified a novel endogenous trigger for autoimmune diabetes and an in vivo role for granzyme A i

98 cells (T regs) are important for preventing autoimmune diabetes and are either thymic-derived (natur

99 nts improves identification of patients with autoimmune diabetes and delineates those who have a more

100 mmatory condition, we examined patients with autoimmune diabetes and demonstrated that these subjects

101 Previous studies in mouse models of autoimmune diabetes and encephalomyelitis have indicated

102 e conclude that TRAIL deficiency accelerates autoimmune diabetes and enhances autoimmune responses.

103 NOD mice develop type 1 autoimmune diabetes and exhibit genetically dominant res

104 alactosylceramide (alphaGalCer), ameliorates autoimmune diabetes and experimental autoimmune encephal

105 epistatic mechanisms in the manifestation of autoimmune diabetes and further indicate the utility of

106 red with measuring Abs improves detection of autoimmune diabetes and how beta-cell function correlate

107 DC expansion is sufficient to prevent type 1 autoimmune diabetes and IBD, which suggests that interfe

108 IL-35 could be used as a potent inhibitor of autoimmune diabetes and implicate its potential therapeu

109 l in preventing the onset and progression of autoimmune diabetes and in promoting islet graft surviva

110 Prevention of autoimmune diabetes and induction of islet transplantati

111 rovide novel insights into the mechanisms of autoimmune diabetes and may lead to development of novel

112 l for specific treatment of diseases such as autoimmune diabetes and pancreatic cancer.

113 ole genome analyses and verified by Q-PCR in autoimmune diabetes and performed a hierarchical cluster

114 er than hematopoietic cells protects against autoimmune diabetes and point to a novel role for PD-1-P

115 se findings identify a Tfh cell signature in autoimmune diabetes and suggest that this population cou

116 s in innate immunity influence the course of autoimmune diabetes and support the use of targeted stra

117 tolerance alone can protect NOD8.3 mice from autoimmune diabetes and that profound changes in T-cell

118 ther the role of FasL in the pathogenesis of autoimmune diabetes and to determine whether gld-induced

119 iling Treg activity, Flicr markedly promotes autoimmune diabetes and, conversely, restrains antiviral

120 es in nonobese diabetic (NOD) mice prevented autoimmune diabetes and, importantly, reversed disease i

121 ice treated with AZD1480 were protected from autoimmune diabetes, and diabetes was reversed in newly

122 ing CD4(+) and CD8(+) T cell function during autoimmune diabetes, and thus may contribute to limiting

123 ic (NOD) mice, which are used to model human autoimmune diabetes, are resistant to costimulation bloc

124 Young-onset autoimmune diabetes associated with additional autoimmun

125 letion of T cell CD98 prevented experimental autoimmune diabetes associated with dramatically reduced

126 pletely protects nonobese diabetic mice from autoimmune diabetes but also causes massive double-negat

127 le B7-2 (NOD-B7-2KO mice) are protected from autoimmune diabetes but develop a spontaneous autoimmune

128 critical K(b)/A12-21 epitope) did not induce autoimmune diabetes but elicited a systemic Foxp3(+) CD2

129 tpn22 knockdown did not increase the risk of autoimmune diabetes but, rather, conferred protection fr

130 bout 2% of LEW*1WR1 rats develop spontaneous autoimmune diabetes, but disease penetrance is much high

131 -CD3 is a promising therapeutic approach for autoimmune diabetes, but its mechanism of action remains

132 -CD3 treatment to be a promising therapy for autoimmune diabetes, but its mechanism of action remains

133 perplasia occurs following immune therapy of autoimmune diabetes, but the clinical remission soon aft

134 lls) are known to control the progression of autoimmune diabetes, but when, where, and how they exert

135 t that PTM contributes to the progression of autoimmune diabetes by eliciting T-cell responses to new

136 that IL-7 contributes to the pathogenesis of autoimmune diabetes by enabling T(E/M) cells to remain i

137 D model, reduced thymic deletion ameliorates autoimmune diabetes by increasing Tregs.

138 ating lymphoid organogenesis, Bcl-3 prevents autoimmune diabetes by inhibiting inflammatory chemokine

139 Thus, T reg cells primarily impinge on autoimmune diabetes by reining in destructive T cells in

140 It may be possible to prevent autoimmune diabetes by targeting a limited element of th

141 A(g7), in the NOD mouse model of spontaneous autoimmune diabetes, confers diabetes risk by modulating

142 to substantial, long-term protection against autoimmune diabetes, despite limited intraislet IL-35 se

143 hance encephalomyelitis, but did inhibit the autoimmune diabetes developing spontaneously in nonobese

144 ts gradually lose their VTCN1 protein during autoimmune diabetes development despite upregulation of

145 Spontaneous autoimmune diabetes development in NOD mice requires bot

146 ffects of hyperbaric oxygen therapy (HOT) on autoimmune diabetes development in nonobese diabetic (NO

147 lymphocytic choriomeningitis virus or during autoimmune diabetes development in the CD8-driven lympho

148 autologous transfer of DN T cells can impede autoimmune diabetes development, at least in the 3A9 TCR

149 reveals that CD103(+) DCs are essential for autoimmune diabetes development.

150 a critical self-antigen in animal models of autoimmune diabetes, due to extremely limited access to

151 d is sufficient to prevent the recurrence of autoimmune diabetes following islet transplantation.

152 unotherapy, an approach to selectively block autoimmune diabetes, generally declines in nonobese diab

153 Autoimmune diabetes has been difficult to study or treat

154 Effector function of T cells in autoimmune diabetes has been widely studied with mixed p

155 es (Idd) intervals that confer resistance to autoimmune diabetes have been identified in mice and hum

156 Current interventions for arresting autoimmune diabetes have yet to strike the balance betwe

157 ine if these patients, like animal models of autoimmune diabetes, have an early and severe loss of is

158 Using a transgenic model of autoimmune diabetes, here we show that ablation of TGF-b

159 itis is an important pathological feature of autoimmune diabetes; however, mechanisms governing the r

160 cells are functionally capable of promoting autoimmune diabetes if they have a critical autoimmune s

161 These SLEC-like cells were able to trigger autoimmune diabetes in a susceptible background.

162 etiopathological relationship between latent autoimmune diabetes in adults (LADA) and classical type

163 differed from that in GAD65Ab-positive late autoimmune diabetes in adults (LADA) patients (n = 44),

164 Latent autoimmune diabetes in adults (LADA) usually refers to G

165 (16p13.13) were convincingly associated with autoimmune diabetes in adults (P </= 0.002), with consis

166 ent with the hypothesis that the genetics of autoimmune diabetes in adults and children are different

167 dhood-onset type 1 diabetes, the genetics of autoimmune diabetes in adults are not well understood.

168 Latent autoimmune diabetes in adults or type 1.5 diabetes is co

169 ting in hybrid forms of diabetes (eg, latent autoimmune diabetes in adults).

170 vitiligo, autoimmune thyroid disease, latent autoimmune diabetes in adults, rheumatoid arthritis, pso

171 ct of oral anti-CD3 mAb on the prevention of autoimmune diabetes in AKR mice in which the low-dose st

172 the intestinal microbiota as a regulator of autoimmune diabetes in animal models is well-established

173 Nicotinamide prevents autoimmune diabetes in animal models, possibly through i

174 Development of autoimmune diabetes in both humans and mice is preceded

175 ats and reduce the incidence of experimental autoimmune diabetes in diabetes-prone (DP-BB/W) rats.

176 lls is deficient before onset of spontaneous autoimmune diabetes in diabetes-prone BB (BBDP) rats.

177 sure to viruses can affect the penetrance of autoimmune diabetes in genetically susceptible animals.

178 betes, we used a model of viral induction of autoimmune diabetes in genetically susceptible biobreedi

179 ow transplantation has been shown to prevent autoimmune diabetes in heavily irradiated nonobese diabe

180 n (NRAMP1) pathways influence development of autoimmune diabetes in humans and NOD mice.

181 Interestingly, one gene linked to autoimmune diabetes in mouse and human, UBD, lies within

182 AS605240 effectively prevented and reversed autoimmune diabetes in NOD mice and suppressed T-cell ac

183 ed tissues, delayed the onset of spontaneous autoimmune diabetes in NOD mice by inhibiting insulitis

184 hat Pep overexpression in T cells attenuates autoimmune diabetes in NOD mice by preferentially modula

185 for 12/15-LO in conferring susceptibility to autoimmune diabetes in NOD mice through its effects on m

186 of the costimulatory molecule B7-2 prevents autoimmune diabetes in NOD mice, but leads to the develo

187 a-galactosylceramide (alpha-GalCer) inhibits autoimmune diabetes in NOD mice, in part by inducing rec

188 ve recently shown that during progression to autoimmune diabetes in NOD mice, memory autoreactive reg

189 s, NK cells are not required for spontaneous autoimmune diabetes in NOD mice.

190 ential for the initiation and development of autoimmune diabetes in NOD mice.

191 hocytes are required for the pathogenesis of autoimmune diabetes in NOD mice.

192 candidate gene (in the Idd9.3 interval) for autoimmune diabetes in NOD mice.

193 allogeneic ADMSC therapy in T cell-mediated autoimmune diabetes in NOD mice.

194 oreactive CD4 T cells are key for initiating autoimmune diabetes in NOD mice; however, little is know

195 e purified diabetic T cells failed to elicit autoimmune diabetes in NOD/beta2m mice.

196 ells obtained from diabetic NOD mice induced autoimmune diabetes in NOD/scid and NOD/CIIT mice, but t

197 similar regimen prevented the recurrence of autoimmune diabetes in NOD/severe combined immunodeficie

198 -induced herpes stromal keratitis and murine autoimmune diabetes in non-obese diabetic (NOD) mice.

199 B. dorei LPS does not decrease incidence of autoimmune diabetes in non-obese diabetic mice.

200 perimental autoimmune encephalomyelitis, and autoimmune diabetes in non-obese diabetic mice.

201 Most treatments that prevent autoimmune diabetes in nonobese diabetic (NOD) mice requ

202 ) or FasL (called the gld mutation) prevents autoimmune diabetes in nonobese diabetic (NOD) mice, the

203 R-Vbeta13, is required for susceptibility to autoimmune diabetes in rats, and selective depletion of

204 usage is a determinant of susceptibility to autoimmune diabetes in rats.

205 onistic Ab against PD-1 provoked destructive autoimmune diabetes in RIP-mOVA mice expressing chicken

206 Finally, BTLA(-/-) OT-I cells caused autoimmune diabetes in RIP-mOVA recipient mice.

207 eases and is involved in the pathogenesis of autoimmune diabetes in the BB/Wor animal model of the di

208 in KRV-induced innate immune activation and autoimmune diabetes in the BBDR rat.

209 atory T (T reg) cells control progression to autoimmune diabetes in the BDC2.5/NOD mouse model by rei

210 n is the underlying cause of lymphopenia and autoimmune diabetes in the BioBreeding (BB) rat.

211 These results suggest that autoimmune diabetes in the NOD may not be a Th1-driven d

212 ia genetically engineered B cells to prevent autoimmune diabetes in the NOD mouse (see the related ar

213 e regulation of induction and progression of autoimmune diabetes in the NOD mouse and provide the rat

214 iabetes (Idd) loci modify the progression of autoimmune diabetes in the NOD mouse, an animal model of

215 The development of autoimmune diabetes in the nonobese diabetic (NOD) mouse

216 provide insight into the polygenic nature of autoimmune diabetes in the rat and the interplay of gene

217 or antigen specificity during progression of autoimmune diabetes in the unmanipulated NOD mouse.

218 OXP3, both in vitro and in a murine model of autoimmune diabetes in vivo.

219 T cell clones closely resembles spontaneous autoimmune diabetes in which both CD4 and CD8 T cells ar

220 the Fas gene in a transgenic model of type 1 autoimmune diabetes in which CD4+ T cells with a transge

221 analyzed HLA class II genotypes, markers of autoimmune diabetes, in 187 children with permanent diab

222 develop insulin autoantibodies, insulitis or autoimmune diabetes, in contrast with mice containing at

223 amplification loop during the progression of autoimmune diabetes, in which initial T cell infiltratio

224 HOT reduces autoimmune diabetes incidence in NOD mice via increased

225 be involved in leukocyte recruitment during autoimmune diabetes, including members of the leukocyte

226 of Toso(-/-) dendritic cells did not induce autoimmune diabetes, indicating their tolerogenic potent

227 Autoimmune diabetes, insulitis, and the infiltrating cel

228 One seminal aspect in autoimmune diabetes is antigen presentation of beta cell

229 Autoimmune diabetes is believed to be mediated primarily

230 Autoimmune diabetes is characterized by inflammatory inf

231 Susceptibility to type 1A autoimmune diabetes is linked to expression of particula

232 hypothesized that enhanced susceptibility to autoimmune diabetes is the result of targeting of insuli

233 involvement in promoting the development of autoimmune diabetes is unknown.

234 The diversity of Ags targeted by T cells in autoimmune diabetes is unknown.

235 estion about the pathogenesis of spontaneous autoimmune diabetes is whether there are primary autoant

236 disorder associated with juvenile onset non-autoimmune diabetes mellitus and progressive optic atrop

237 lls to provide insight into TCR diversity in autoimmune diabetes mellitus.

238 In the autoimmune diabetes model, whole spleen cells obtained f

239 deficiency in type 1 diabetes and in rodent autoimmune diabetes models is caused by beta-cell-specif

240 ll-destructive process using two independent autoimmune diabetes models, an inducible autoantigen-spe

241 ons were observed in induced and spontaneous autoimmune diabetes models, became apparent at diabetes

242 nsion in both collagen-induced arthritis and autoimmune diabetes mouse models.

243 transform a "regulated predisposition" into autoimmune diabetes, namely, failure to maintain regulat

244 Autoimmune diabetes occurs when invading lymphocytes des

245 = 12), type 2 diabetes (T2D, n = 31), latent autoimmune diabetes of adults (LADA, n = 6) and type 1 d

246 ted GAD65 to patients classified with latent autoimmune diabetes of the adult (LADA) is safe and sugg

247 nsulin B:9-23), is central to development of autoimmune diabetes of the NOD mouse model.

248 highly active in antigen presentation in the autoimmune diabetes of the NOD mouse: they do this by pr

249 lity complex (MHC) class II molecules in the autoimmune diabetes of the nonobese diabetic (NOD) mouse

250 hypomorph that causes profoundly accelerated autoimmune diabetes on a NOD background.

251 of diabetes-resistant BB rats, which develop autoimmune diabetes only after perturbation of the immun

252 e, nonobese diabetic (NOD) mice, but delayed autoimmune diabetes only in the former.

253 c) allele) for susceptibility to spontaneous autoimmune diabetes, or to diabetes elicited by reciproc

254 udy provides a novel natural system to study autoimmune diabetes pathogenesis and reveals a previousl

255 mmary, ADMSC therapy efficiently ameliorates autoimmune diabetes pathogenesis in diabetic NOD mice by

256 Autoantigen-based immunotherapy can modulate autoimmune diabetes, perhaps due to the activation of Ag

257 d IGF-I expression in mouse liver suppressed autoimmune diabetes progression.

258 ed mice that lack cathepsin L (Cat L) on the autoimmune diabetes-prone NOD inbred background.

259 We found that a fraction of young autoimmune diabetes-prone NOD mice had elevated levels o

260 a-cell line were implanted subcutaneously in autoimmune diabetes-prone NOD mice, beta-cell-reactive T

261 a genetically disrupted CD38 allele into the autoimmune diabetes-prone NOD/Lt background accelerated

262 estigated the potential of LSF in preventing autoimmune diabetes recurrence after islet transplantati

263 This study demonstrates that autoimmune diabetes recurrence after islet transplantati

264 the importance of Fas in the development of autoimmune diabetes remains controversial.

265 Indeed, previous findings in autoimmune diabetes revealed a feedback mechanism that r

266 In this model of spontaneous autoimmune diabetes, secondary lymphoid structures, most

267 orts to induce and maintain tolerance in the autoimmune diabetes setting by using therapeutic vaccina

268 In the NOD mouse model of autoimmune diabetes, several beta cell-cytotoxic CD8 T c

269 In autoimmune diabetes, short course treatment with FcR-non

270 esolution maps of pancreatic inflammation in autoimmune diabetes should prove invaluable in assessing

271 th R3 insulin-IA(g7) complexes would inhibit autoimmune diabetes specifically without interfering wit

272 nity TCRs could mediate potent insulitis and autoimmune diabetes, suggesting that TCR affinity does n

273 Autoimmune diabetes (T1D) is characterized by CD4(+) T c

274 Biobreeding (BB) rats model type 1 autoimmune diabetes (T1D).

275 ice were, paradoxically, more susceptible to autoimmune diabetes than wild-type mice.

276 depletes and reprograms B-cells and reverses autoimmune diabetes, thereby providing a blueprint for d

277 of Itgb2 or ItgaL confers protection against autoimmune diabetes through distinctly different mechani

278 role for CD137 acting in the early phase of autoimmune diabetes to enhance regulatory cell productio

279 ffective in T cell-mediated diseases such as autoimmune diabetes to generate Ag-specific immunosuppre

280 for development of CD8 lymphocyte-dependent autoimmune diabetes (type 1 diabetes [T1D]) in the rat i

281 he parvovirus Kilham rat virus (KRV) develop autoimmune diabetes via a mechanism that does not involv

282 nd IFN-gamma appears completely different in autoimmune diabetes vs neuropathy.

283 Notably, autoimmune diabetes was exacerbated in NOD.MerTK(KD/KD)

284 s was impaired, and (iii) the development of autoimmune diabetes was significantly reduced.

285 In this study, using a mouse model of autoimmune diabetes, we aimed to determine the means by

286 of proinsulin, which plays a pivotal role in autoimmune diabetes, we found that targeting to the ER h

287 tudy the role of RAGE/ligand interactions in autoimmune diabetes, we tested the ability of soluble RA

288 munomodulatory candidate because it prevents autoimmune diabetes when expressed in beta cells or subc

289 OVA in pancreatic beta cells, develop severe autoimmune diabetes when given OT-I cells (OVA-specific

290 ective in blocking the onset and the ongoing autoimmune diabetes, whereas CD28/CD154 blockade has no

291 that mature DC (mDC) prevented the onset of autoimmune diabetes, whereas immature DC (iDC) were ther

292 f 6.9TCR transgenic mice provides a model of autoimmune diabetes whereby controlled expression of an

293 reveals a unique protective role of c-Rel in autoimmune diabetes, which is distinct from other T-cell

294 mouse strain is that it develops spontaneous autoimmune diabetes, which shares many similarities to a

295 significantly lower incidence of spontaneous autoimmune diabetes, which was accompanied by fewer IFN-

296 Nonobese diabetic (NOD) mice develop autoimmune diabetes with features similar to those obser

297 we show that the Fas-deficient mice develop autoimmune diabetes with slightly accelerated kinetics i

298 onobese diabetic mice developing spontaneous autoimmune diabetes) with beta cell-specific expression

299 ly, partial disruption of FasL protects from autoimmune diabetes without causing T-cell lymphoprolife

300 ets facilitates beta-cell destruction during autoimmune diabetes, yet specific mechanisms governing t