ライフサイエンスコーパス: diabetogenic

1 ng those recently found to be obesogenic and diabetogenic.

2 killing human beta cells and thereby may be diabetogenic.

3 ion, many of the immunosuppressive drugs are diabetogenic.

4 transgenic splenocytes exhibited attenuated diabetogenic ability.

5 f fasting blood glucose and responded to the diabetogenic action of streptozotocin.

6 bone marrow chimerism approaches tested the diabetogenic activity of CD4 and CD8 T-cells from NOR mi

7 on on chromosome 4 was found to diminish the diabetogenic activity of CD4 but not CD8 T-cells.

8 e(s) within the Idd9/11 region regulates the diabetogenic activity of CD4 T-cells.

9 We compared KRV with other viruses for diabetogenic activity.

10 /10 strains were characterized by suppressed diabetogenic activity.

11 Streptozotocin (STZ) is a diabetogenic agent extensively used to induce diabetes a

12 Streptozotocin (STZ) is widely used as diabetogenic agent in animal models for diabetic nephrop

13 mpaired in rats depleted of insulin with the diabetogenic agent streptozotocin (STZ).

14 5or-/- mice have enhanced sensitivity to the diabetogenic agent streptozotocin.

15 difying effects of obesity, autoimmunity, or diabetogenic agents like streptozotocin may confound und

16 for HGF/c-Met in beta-cell survival against diabetogenic agents.

17 CD8(+) T cells transgenically expressing the diabetogenic AI4 T-cell receptor adoptively transferred

18 CD8 T-cells transgenically expressing the diabetogenic AI4 TCR were transferred into 91 (NODxB6.H2

19 splantation was critical for tolerization of diabetogenic and alloreactive host T-cells.

20 sulin II promoter (RIP) are resistant to the diabetogenic and cytotoxic effects of streptozotocin (ST

21 iferation (threefold), and resistance to the diabetogenic and cytotoxic effects of streptozotocin com

22 OD) mice, as well as NOD mice coexpressing a diabetogenic and I-A(g7)-restricted, but MHC-promiscuous

23 By combining diabetogenic and nondiabetogenic or nonautoantigen-speci

24 rly to examine the effect of B cells on both diabetogenic and regulatory Ag-specific T cells, we gene

25 B chain epitopes necessary for activation of diabetogenic anti-insulin BDC12-4.1 T cells, indicating

26 e conclude that in NOD mice, ZnT8 is a minor diabetogenic antigen that can participate in diabetes in

27 ogenic" antigen-presenting cells pulsed with diabetogenic antigens and transfer of induced or expande

28 in NOD mice, the identity of the primordial diabetogenic antigens, and our understanding of the bala

29 loss of NOX-derived superoxide would dampen diabetogenic antiviral macrophage responses and protect

30 ost likely responsible for the generation of diabetogenic APC in NOD mice.

31 significantly refine genetic loci regulating diabetogenic B and CD4 T cell activity.

32 nd to contain the main NOR gene(s) dampening diabetogenic B cell activity, with Ephb2 and/or Padi2 be

33 ful in dissecting the developmental basis of diabetogenic B-lymphocytes.

34 ) NOD mice showed similar frequencies of the diabetogenic BDC 2.5 CD4(+) T cells.

35 iabetes mediated by the adoptive transfer of diabetogenic BDC2.5 CD4(+) T cells.

36 cells and inhibit in vitro proliferation of diabetogenic BDC2.5 cells.

37 erived gal-1-DC triggered rapid apoptosis of diabetogenic BDC2.5 TCR-transgenic CD4+ T cells by TCR-d

38 Accordingly, diabetogenic BDC2.5 Th17 cells were transferred into NOD

39 Nod.scid recipients of diabetogenic BDC2.5.NOD cells were protected indefinitel

40 Our data indicate that Tc17 cells are not diabetogenic but can potentiate a Th1-mediated disease.

41 The BDC2.5 T cell clone is highly diabetogenic, but the transgenic mouse generated from th

42 ive CD8(+) lymphocytes might determine their diabetogenic capacity by affecting recruitment of cells

43 election, activation, and development of the diabetogenic capacity of these insulin-reactive T-cells.

44 9(-/-) CD8 T cells had significantly reduced diabetogenic capacity, whereas absence of CD137 in non-T

45 To determine where T reg cells affect the diabetogenic cascade, we crossed the Foxp3 scurfy mutati

46 us, IRF5 is a crucial downstream mediator of diabetogenic CB1R signaling in macrophages and a potenti

47 und that Gr1(+)CD11b(+) cells could suppress diabetogenic CD4 and CD8 T cell function in an IL-10-, N

48 tide (IAPP) to be the target Ag for a highly diabetogenic CD4 T cell clone BDC-5.2.9.

49 Using a panel of diabetogenic CD4 T cell clones derived from the NOD mous

50 iously that after migration to the pancreas, diabetogenic CD4 T cell clones produce a variety of infl

51 Diabetogenic CD4 T cell clones produce several inflammat

52 generation of self-peptide ligands directing diabetogenic CD4 T cell development.

53 ial insulin epitope (B:9-23) is presented to diabetogenic CD4 T cells by IA(g7) in a weakly bound reg

54 events that lead to specific localization of diabetogenic CD4 T cells into islets of Langerhans resul

55 Here, we report that the entry of diabetogenic CD4 T cells very rapidly triggered inflamma

56 In contrast to the entry of diabetogenic CD4 T cells, the entrance of nonspecific T

57 stocompatibility molecules and activation of diabetogenic CD4 T cells.

58 IAPP is the target antigen for the diabetogenic CD4 T-cell clone BDC-5.2.9.

59 as the antigen target for three NOD-derived, diabetogenic CD4 T-cell clones, including the well-known

60 tion both in vitro and in vivo in a panel of diabetogenic CD4 Th1 T cell clones derived from the NOD

61 Adoptive transfer of diabetogenic CD4 Th1 T cell clones into young NOD or NOD

62 entary to our in vivo approach, coculture of diabetogenic CD4(+) and CD8(+) T cells with NOD.RAG1(-/-

63 Adoptive transfer of diabetogenic CD4(+) and CD8(+) T cells, but not B cells,

64 e NKT cells, were sufficient to downregulate diabetogenic CD4(+) BDC2.5 NOD T cells in adoptive trans

65 temic trafficking and tissue localization of diabetogenic CD4(+) BDC2.5 T (BDC) cells in recipient mi

66 omogranin A (ChgA) as the antigen for highly diabetogenic CD4(+) T cell clones.

67 However, how PD-1 influences diabetogenic CD4(+) T cells during natural diabetes is n

68 insulin B chain contains a major epitope for diabetogenic CD4(+) T cells in the NOD mouse model of ty

69 They failed to induce proliferation of diabetogenic CD4(+) T cells in vitro.

70 uce Th2 responses when cultured ex vivo with diabetogenic CD4(+) T cells obtained from BDC2.5 TCR tra

71 at autocrine/paracrine TGF-beta signaling in diabetogenic CD4(+) T cells, but not Treg cells, is esse

72 The diabetogenic CD4(+)BDC2.5 (BDC) T cell clone upon transf

73 a transfer model of acute diabetes using the diabetogenic CD4+ BDC2.5 T-cell clone was established.

74 Both of these peptides are targets of diabetogenic CD4+ T cell clones in the nonobese diabetic

75 To understand better how diabetogenic CD4+ T cells induce islet beta-cell death a

76 t NKT cells efficiently dampen the action of diabetogenic CD4+ T cells, and do so in an indirect mann

77 ccompanied by an age-dependent increase in a diabetogenic CD8 clonotype.

78 e transgenically expressing the TCR from the diabetogenic CD8 T cell clone AI4 with NOD stocks congen

79 nteractive non-MHC genes allow a NOD-derived diabetogenic CD8 T cell clonotype (AI4) to be negatively

80 Adoptive transfer of a diabetogenic CD8 T cell population (AI4) induced a high

81 ted with both enhanced negative selection of diabetogenic CD8 T cells and increased aggressiveness of

82 r, it was unknown whether the development of diabetogenic CD8 T cells could also be dominantly inhibi

83 nic APCs, which led to reduced activation of diabetogenic CD8 T cells.

84 We have previously reported a highly diabetogenic CD8 T-cell clone, G9C8, in the nonobese dia

85 acting gene(s) that can promote autoreactive diabetogenic CD8 T-cell responses.

86 ivered a mimotope peptide, recognized by the diabetogenic CD8(+) T cell clone AI4, to DCs in NOD mice

87 ses how IFN-gamma can suppress activation of diabetogenic CD8(+) T cells.

88 ed from any lymphocyte source and suppressed diabetogenic CD8(+) T-cell responses both directly and t

89 compare their susceptibility to cytolysis by diabetogenic CD8(+) T-cells in vitro.

90 selectively target a prevalent population of diabetogenic CD8(+) T-cells that contribute to the progr

91 molecules can mediate the thymic deletion of diabetogenic CD8+ T cells as illustrated using the AI4 T

92 hoid cells, which prevented the expansion of diabetogenic CD8+ T cells expressing programmed cell dea

93 that may explain this behavior, we analyzed diabetogenic CD8+ T cells that recognize a peptide from

94 teractively impair the negative selection of diabetogenic CD8+ T cells.

95 hoid organs of FTY720-treated mice contained diabetogenic cells but not dominant immunoregulatory cel

96 locked diabetes by inhibiting the priming of diabetogenic cells in the pancreatic lymph nodes and the

97 sensitivity of these cells to destruction by diabetogenic cells in vivo.

98 When cotransferred with diabetogenic cells into NOD scid recipients, T regs indu

99 crease individual exposure to obesogenic and diabetogenic chemicals.

100 Thus, diabetogenic class II MHC molecules are highly selective

101 t fratricide of beta-cells after transfer of diabetogenic clones.

102 Under diabetogenic conditions, MDM2 and p53 are upregulated, w

103 Under diabetogenic conditions, MST1 was strongly activated in

104 regulating beta-cell function in normal and diabetogenic conditions.

105 the dynamic behavior of a virally expanded, diabetogenic CTL population in the pancreas at cellular

106 yperglycemia, and therapy was shown to alter diabetogenic cytokine profile, to diminish T-cell effect

107 del of obesity/metabolic syndrome, feeding a diabetogenic diet high in saturated fat and refined carb

108 -) mice were placed on high-fat-high-sucrose diabetogenic diet or control diet for 24 weeks.

109 a model AD-type amyloid neuropathology) to a diabetogenic diet that promotes IR results in a ~2-fold

110 by feeding a high-fat, high-sucrose, type-2 diabetogenic diet to C57BL/6J mice for 8 mo.

111 ulin levels than apoE(+/+) mice when fed the diabetogenic diet.

112 o improved in mice lacking apoE when fed the diabetogenic diet.

113 significantly increased in apoE(-/-) mice on diabetogenic diet.

114 in Cohen diabetes-sensitive (CDs) rats fed a diabetogenic-diet (CDs-HSD).

115 r explore potential mechanisms through which diabetogenic dietary conditions that result in promotion

116 receptor (LDLR)-deficient mice fed high fat diabetogenic diets (HFD).

117 Following the administration of the diabetogenic drug streptozotocin, rats selecting their d

118 ndings are reassuring as they did not show a diabetogenic effect of a six-month supplementation with

119 However, the mechanisms for the diabetogenic effect of iAs are still largely unknown.

120 e the incretin effect and buffer against the diabetogenic effect of inherent glucagon activity.

121 Although historically thought to have little diabetogenic effect, there is growing evidence of beta-c

122 evaluating the pathogenic potential of human diabetogenic effector cells in vivo.

123 tory T cell numbers that efficiently lowered diabetogenic effector memory T cells.

124 The in vivo anti-diabetogenic effects occur at a dose substantially lower

125 To investigate the potential diabetogenic effects of NF-kappaB in beta-cells, we gene

126 in pancreas recipients because it avoids the diabetogenic effects of steroids.

127 ies have thoroughly reported on the combined diabetogenic effects of variants in the two regions.

128 benefits of corticosteroids because of their diabetogenic effects.

129 Although the diabetogenic encephalomyocarditis strain D virus induces

130 is study a glutamic acid decarboxylase (GAD) diabetogenic epitope was expressed on an Ig to enhance t

131 he hypothesis that exposure to POPs may be a diabetogenic factor in both obese and nonobese individua

132 ce, locally produced apoCIII is an important diabetogenic factor involved in impairment of beta-cell

133 t may therefore be controlled, in part, by a diabetogenic factor(s), perhaps unrelated to the Gimap5

134 ificant lifestyle effects on atherogenic and diabetogenic fat depots.

135 ely, our results indicate that one important diabetogenic function of CD137 is to promote the expansi

136 endent T1D susceptibility by controlling the diabetogenic function of islet-specific CD4(+) T cells.

137 tive responses to endogenous autoantigen and diabetogenic function were impaired in BDC-Idd9.905 CD4(

138 cyclin-dependent kinase 5 (Cdk5) stimulates diabetogenic gene expression in adipose tissues.

139 n transferred together with small numbers of diabetogenic HA-specific CD4+ T cells, a strikingly diff

140 Consumption of a diabetogenic high-fat diet causes the partitioning and a

141 early stages of atherosclerosis when fed a "diabetogenic" high fat diet.

142 rived peptides were identified as targets of diabetogenic HLA-A*0201-restricted T cells in our NOD tr

143 ely identical to a primary target epitope of diabetogenic HLA-A2-restricted CD8 T cells.

144 y translatable interventions for suppressing diabetogenic HLA-A2.1-restricted T-cell responses.

145 ning preserves alloreactive and autoreactive diabetogenic host NOD T-cells, but when mixed chimerism

146 from pancreatic islet beta-cells selected by diabetogenic I-A(g7) molecules of NOD mice.

147 T cells, we crossed NOD-IGRP mice to highly diabetogenic IGRP206-214 T-cell receptor transgenic mice

148 essential for initiating and maintaining the diabetogenic immune response.

149 fectively protect pancreatic beta-cells from diabetogenic immune responses.

150 onor brain death, longer cold ischemia time, diabetogenic immunosuppression, and auto- and alloimmuni

151 Ccl11 (Eotaxin), previously postulated to be diabetogenic in BBDR rats, a BBDP-related strain.

152 ng the CD40 receptor (Th40 cells) are highly diabetogenic in NOD mice, and NOD.BDC2.5.TCR.Tg mice pos

153 nsfer models, islet-specific Th17 cells were diabetogenic independently of IL-17 and displayed inflam

154 However, a highly diabetogenic insulin B chain epitope within the B:9-23 p

155 D44 receptor is critical for the adhesion of diabetogenic insulin-specific, CD8-positive, K(d)-restri

156 that have examined T cells in pancreas, the diabetogenic insulitis lesion, and lymphoid tissues have

157 ed insulin secretion and may be perturbed by diabetogenic insults to disrupt glucose homeostasis in h

158 g both their proliferation and production of diabetogenic interferon-gamma.

159 Liver-directed T3 action offsets the diabetogenic liability of glucagon, and glucagon-mediate

160 regulate bone growth, but at the expense of diabetogenic, lipolytic, and hepatosteatotic consequence

161 tive and informative biomarkers for studying diabetogenic mechanisms, assessing preonset risk, and mo

162 Here, we have shown that diabetogenic MHC class II molecules bound to a peptide w

163 Diabetogenic MHC class II molecules, such as human HLA-D

164 tive CD4(+) and CD8(+) T cells restricted by diabetogenic MHC molecules in an I-E-independent manner.

165 betogenic spleen cells as well as the highly diabetogenic monoclonal BDC2.5 TCR transgenic T cells th

166 ave compared mice heterozygous for the Akita diabetogenic mutation (Akita) with mice homozygous for t

167 athy in male mice heterozygous for the Akita diabetogenic mutation in the insulin 2 gene (Ins2).

168 /-) inbred males carrying the dominant Akita diabetogenic mutation Ins2(C96Y/+).

169 The diabetogenic nature and homing properties of purified bo

170 is study reveals the gut microbiome-mediated diabetogenic nature of organophosphates and hence that t

171 The diabetogenic nature of organophosphates was recently rep

172 ere backcrossed five to eight times onto the diabetogenic NONcNZO10/Ltj background.

173 lying uncomplicated obesity syndromes versus diabetogenic obesity (diabesity) syndromes.

174 Effector differentiation of diabetogenic OT-I CD8+ T cells is enhanced in rat insuli

175 eks and have increased susceptibility to the diabetogenic oxidant streptozotocin.

176 - and NOD IFN-gamma-/-, respectively) with a diabetogenic, pancreatropic Edwards strain of CVB4.

177 s induction by a subsequent injection of the diabetogenic pCI/ppins.

178 the stage for rational testing of potential diabetogenic peptide epitopes.

179 intake was undetectable in men who harbored diabetogenic polymorphisms of the TCF7L2 gene.

180 as well as enhanced T cell proliferation and diabetogenic potency.

181 ns produced a hierarchy of insulitogenic and diabetogenic potential (BDC-2.5 > NY4.1 > BDC-6.9), whil

182 y, we investigated the factors governing the diabetogenic potential of autoreactive CD8(+) clones iso

183 erance mechanisms selectively impinge on the diabetogenic potential of high-affinity TCRs, mitigating

184 ll E3 genes must be expressed to inhibit the diabetogenic potential of NOD immune cells.

185 ostimulation blockade, despite the continued diabetogenic potential of their T-cells.

186 ssed beta-cell antiviral defense reveals the diabetogenic potential of two pathogens previously linke

187 es not exclusively dictate or correlate with diabetogenic potential.

188 ese findings inform our understanding of the diabetogenic process and reveal new avenues for therapeu

189 viral infections may prevent or trigger the diabetogenic process remains unclear.

190 autoreactivity as a seminal component in the diabetogenic process.

191 re, analyses of K(IR)6.2-based channels with diabetogenic receptors reveal that MgATP-dependent hyper

192 apy that not only selectively suppresses the diabetogenic response and efficiently reverses diabetes,

193 cific T cells is one approach to monitor the diabetogenic response in at risk or diabetic individuals

194 e transporter aberrations, insulin-resistant diabetogenic responses, and distinct chromosomal and chr

195 e investigated whether the molecule inhibits diabetogenic responses.

196 Hence, we postulated a diabetogenic role for defects in the tolerance mechanism

197 In addition, the diabetogenic role of glucagon released from alpha-cells

198 We aimed to identify the diabetogenic secretory product(s) of pancreatic cancer.

199 ng immune protection with strategies lacking diabetogenic side effects.

200 Moreover, patients harboring a diabetogenic SNP in the Clec16a gene have reduced islet

201 receptor (TCR), which is representative of a diabetogenic specificity that is naturally present in NO

202 ive transfer of disease caused by polyclonal diabetogenic spleen cells as well as the highly diabetog

203 s diabetes caused by simultaneously injected diabetogenic splenocytes in NOD-Rag(-/-) mice.

204 e suppressed adoptive transfer of disease by diabetogenic splenocytes into secondary immunodeficient

205 The co-transfer of diabetogenic splenocytes with splenocytes from anti-CD4

206 rthermore, these mice were protected against diabetogenic stimuli that cause oxidative stress damage

207 Hence, ALR/Lt islets resist cytokine-induced diabetogenic stress through enhanced dissipation and/or

208 trating cells after adoptive transfer by the diabetogenic T cell clone BDC-2.5 indicates that large n

209 ity, stimulus for the spontaneously arising, diabetogenic T cell clone BDC2.5.

210 Insulin epitopes recognized by diabetogenic T cell clones bind poorly to the class II I

211 (+)CD11b(+) cells not only directly suppress diabetogenic T cell function but also can induce regulat

212 ity in type 1 diabetes, but also in altering diabetogenic T cell function ex vivo for therapy.

213 Further analyses showed that diabetogenic T cell function was modulated primarily thr

214 wed that the tetramer(+) T cells could block diabetogenic T cell migration into lymph nodes.

215 Cat L-deficient mice, although a potentially diabetogenic T cell repertoire persists.

216 milar to NOD mice, NOD.DO animals selected a diabetogenic T cell repertoire, and the numbers and func

217 mechanisms converge to shape and broaden the diabetogenic T cell repertoire, potentially complicating

218 s that exert regulatory activity suppressing diabetogenic T cell responses.

219 with EXOs promoted expansion of transferred diabetogenic T cells and accelerated the effector T cell

220 ification of epitopes that are recognized by diabetogenic T cells and cause selective beta cell destr

221 ce by CA treatment reduces the activation of diabetogenic T cells and impedes type 1 diabetes onset v

222 nt in the NOD mouse-disease transferred with diabetogenic T cells and recurrent disease in NOD/scid r

223 uced transient aggressive behavior in BDC2.5 diabetogenic T cells and reduction in T(reg) cell number

224 rtoire, thereby preventing the activation of diabetogenic T cells and subsequent diabetes development

225 ts interactively regulate the development of diabetogenic T cells and the TCR promiscuity of such aut

226 microscopy to analyze lymph node priming of diabetogenic T cells and to delineate the mechanisms of

227 ells at early stages of the disease when the diabetogenic T cells are already activated.

228 gerhans permits the specific localization of diabetogenic T cells at a time when there is no inflamma

229 st, recipients of 10 d or older thymi lacked diabetogenic T cells but developed severe colitis marked

230 dulating TCR signaling-mediated functions in diabetogenic T cells but not in T(regs).

231 s not a requirement for islet entry and that diabetogenic T cells can recruit a heterogeneous bystand

232 n 10-wk-old insulitis-positive animals whose diabetogenic T cells have populated the islets.

233 lso prevent pancreatic islet infiltration by diabetogenic T cells in mouse models of type 1 diabetes,

234 5 T cells could block autoimmunity caused by diabetogenic T cells in NOD mice, whereas 10(5) polyclon

235 abrogates FcgammaR-mediated cross priming of diabetogenic T cells in RIP-mOVA mice, a situation pheno

236 us gld mutation inhibits the accumulation of diabetogenic T cells in the pancreas, without interferin

237 t is necessary for driving the inhibition of diabetogenic T cells in vivo.

238 These studies establish that entry of diabetogenic T cells induces a state of receptivity of i

239 also are instrumental in the localization of diabetogenic T cells into islets.

240 We used the transfer of genetically modified diabetogenic T cells into normal, mutant, and bone marro

241 The transfer of diabetogenic T cells into NOX-deficient NOD.Rag.Ncf1(m1J

242 ancer patents) impedes the transmigration of diabetogenic T cells into the pancreas and protects non-

243 on the endothelium, repressed the homing of diabetogenic T cells into the pancreatic islets, reduced

244 Preventing activation of diabetogenic T cells is critical for delaying type 1 dia

245 and by which subset, homeostatic control of diabetogenic T cells is normally achieved in vivo.

246 ying paper, we find specific localization of diabetogenic T cells only to islets of Langerhans bearin

247 In this report, we confirm that adhesion of diabetogenic T cells promotes the activation of endogeno

248 TGF-beta and that the ability of the target diabetogenic T cells to respond to TGF-beta was crucial.

249 tion, and what downstream effect this has on diabetogenic T cells was unknown.

250 tly influenced the activities of transferred diabetogenic T cells when they were introduced as a mono

251 ouse and indicated that IL-10 encounter with diabetogenic T cells within the islets sustains activati

252 When adoptively transferred along with diabetogenic T cells, activated G206 T cells significant

253 ck the migration of other T cells, including diabetogenic T cells, and inhibit diabetes development.

254 The successfully treated mice retained diabetogenic T cells, but also had substantially increas

255 tes, were also unaffected by the presence of diabetogenic T cells.

256 of proliferation and cytokine production by diabetogenic T cells.

257 ing that GAD may not be a primary target for diabetogenic T cells.

258 ffective even if administered 14 d after the diabetogenic T cells.

259 to dampen the pathogenicity of autoreactive diabetogenic T cells.

260 elopment, potentiating hyperproliferation of diabetogenic T cells.

261 ion, proliferation, and effector function of diabetogenic T cells; reduced insulin-specific T-cell fr

262 reated mice revealed selective reductions in diabetogenic T helper type 1 (Th1) cells in the pancreat

263 Surprisingly, IL-7-deprived diabetogenic T(E/M) cells remained present in the treate

264 ulate TACE-mediated LAG-3 shedding to impede diabetogenic T-cell activation and progression to diseas

265 ion and further increasing the threshold for diabetogenic T-cell activation.

266 we examined the role of SDF-1 regulation of diabetogenic T-cell adhesion to islet microvascular endo

267 on of SDF-1 in negatively regulating NOD/LtJ diabetogenic T-cell adhesion, which may be important in

268 ication of the target antigen for the highly diabetogenic T-cell clone BDC-5.2.9.

269 ransfers, as well as by adoptive transfer of diabetogenic T-cell clones.

270 NOR MSCs were shown to suppress diabetogenic T-cell proliferation via PD-L1 and to suppr

271 amide-induced diabetes, or the activation of diabetogenic T-cell receptor transgenic CD4(+) T cells a

272 hesion, which may be important in regulating diabetogenic T-cell recruitment into islets.

273 Diabetogenic T-cell recruitment into pancreatic islets f

274 expression as an essential regulator of the diabetogenic T-cell response and providing a potential m

275 6.9TCR/NOD, in which the expression of both diabetogenic T-cells and naturally occurring autoantigen

276 ur study demonstrates that a large number of diabetogenic T-cells are present in the bone marrow of f

277 study, we investigated whether autoreactive diabetogenic T-cells are present in the bone marrow of N

278 h nodes and, thereby, to circulating, naive, diabetogenic T-cells for the first time.

279 Diabetogenic T-cells have also been detected in the sple

280 ver, mechanisms governing the recruitment of diabetogenic T-cells into pancreatic islets are poorly u

281 molecules delete or inactivate autoreactive diabetogenic T-cells.

282 The LTbetaR-Ig-treated mice did not contain diabetogenic T-cells.

283 T-cell ligands involved in the activation of diabetogenic T-cells.

284 ice developed diabetes upon inoculation with diabetogenic T-cells.

285 presenting cells most efficiently activating diabetogenic T-cells.

286 evelopment of thymocytes expressing distinct diabetogenic TCRs sharing common specificity in a thymic

287 bese diabetic (NOD)-scid mice expressing the diabetogenic TCRs, BDC2.5 and 4.1, generate clonotype-po

288 synthase may provide a strategy for reducing diabetogenic Th1 cells and preserving beta cell function

289 of the chemokine receptor CXCR3 and prevents diabetogenic Th1 cells from reaching the pancreas, leadi

290 rated that CD137-deficient T-cells were less diabetogenic than their wild-type counterpart when adopt

291 NOR CD4 T-cells were less diabetogenic than those from NOD mice.

292 th, plays a critical role in the function of diabetogenic Tpaths and Tregs.

293 Down-regulation of Skp2 in diabetogenic Tpaths converts them into Foxp3-expressing

294 d spontaneous T1D, and CD4 T cells were more diabetogenic upon adoptive transfer into NOD.Rag recipie

295 ansplacentally treated with PPI-Fc were less diabetogenic upon transfer into NOD.scid recipients.

296 linking oxidative stress, inflammation, and diabetogenic virus infections.

297 either polyinosinic:polycytidylic acid or a diabetogenic virus to induce diabetes.

298 highlighting the possible role of CVB1 as a diabetogenic virus type.

299 Upon infection with a suspected diabetogenic virus, Coxsackievirus B3 (CB3), NOD.Ncf1(m1

300 lls treated with TGF-beta1 plus IL-6 are not diabetogenic, whereas IL-23-treated cells potently induc