ライフサイエンスコーパス: islet allograft

1 e, in that they rejected a second donor-type islet allograft.

2 unction was documented by rejection of human islet allografts.

3 ge and long-term survival of intratesticular islet allografts.

4 ogated long-term survival of intratesticular islet allografts.

5 long-term (>100 day) survival of cardiac and islet allografts.

6 transplant tolerance induction to mismatched islet allografts.

7 rance to SCID recipients of donor-type fresh islet allografts.

8 cipients; the same recipients rejected fresh islet allografts.

9 spleen of recipients long after rejection of islet allografts.

10 rally required for induction of tolerance to islet allografts.

11 they survived longer than renal subcapsular islet allografts.

12 ough perforin, for induction of tolerance to islet allografts.

13 ot appear to be a factor in rejection of the islet allografts.

14 intratesticular, but not renal subcapsular, islet allografts.

15 to skin allograft tolerance also applies to islet allografts.

16 red for the rejection of fully MHC-disparate islet allografts.

17 ed diabetic NOD mice eventually rejected the islet allografts.

18 r to improve the survival and/or function of islet allografts.

19 nt pathways for T cell-mediated rejection of islet allografts.

20 D154 mAb treatment regiment in recipients of islet allografts.

21 cing transplantation tolerance to pancreatic islet allografts.

22 e (c-Rel-/-) as recipients of H-2 mismatched islet allografts.

23 e toward subsequent extrathymic donor strain islet allografts.

24 ted disruption of CD103 to reject pancreatic islet allografts.

25 of increased IL-4 mRNA expression within the islet allografts.

26 ith CS1-peptide led to long-term survival of islet allografts.

27 pecific T cells resulted in rejection of H2b islet allografts.

28 H-2K(b)-specific T cells than either skin or islet allografts.

29 CD8+ T cell-mediated rejection of pancreatic islet allografts.

30 nduce donor-specific tolerance to pancreatic islet allografts.

31 icient (SCID) recipients bearing established islet allografts.

32 OD/Lt mice, enabling them to accept curative islet allografts.

33 jection and promotes permanent acceptance of islet allografts.

34 MDSCs largely lost their ability to protect islet allografts.

35 uently, failed to protect the cotransplanted islet allografts.

36 plays an important role in the rejection of islet allografts.

37 olonged, drug-free engraftment of cynomolgus islet allografts.

38 were rendered diabetic and transplanted with islet allografts.

39 in T cells is required for the rejection of islet allografts.

40 ovide permanent donor-specific protection of islet allografts.

41 igh dose of streptozotocin and then received islet allografts.

42 ed NRG-Akita mice capable of rejecting human islet allografts.

43 bility of the humanized mice to reject human islet allografts.

44 We used skin and islet allografts, a CD8 T cell receptor (TCR) transgenic

45 equirement for IFN-gamma in the induction of islet allograft acceptance after monoclonal antibody the

46 prior to transplant significantly prolonged islet allograft acceptance.

47 CD40/CD154 pathway signals does not prevent islet allograft acute rejection.

48 spite the immune regulation, intratesticular islet allografts all were rejected within 42 days after

49 rginine did not differ significantly between islet allograft and autograft recipients.

50 ansplantation, lymphangiogenesis occurred in islet allografts and in draining lymph nodes.

51 low enhanced posttransplantation survival of islet allografts and inhibition of recurrent autoimmune

52 n cotransferred together with human PBMC and islet allografts and monitored for evidence of rejection

53 permanent engraftment of fully MHC-disparate islet allografts and significantly prolonged survival in

54 t c-Rel is essential for robust rejection of islet allografts and support the idea that strategies th

55 1/CTLA4Ig therapy induced tolerance to fresh islet allografts and their T cells adoptively transferre

56 ce that had received renal subcapsular human islet allografts and were transfused with 1 x 10(7) of h

57 lls had no effect upon survival of healed-in islet allografts, and CD25 cell deletion had no effect u

58 Moreover, Akita mice readily rejected islet allografts, and chronic hyperglycemia had no impac

59 Islet allografts are currently associated with a high ra

60 ansplanted into type 1a diabetic recipients, islet allografts are subject both to conventional allogr

61 Islet allografts are subject to rapid rejection through

62 al for prolonged survival of intratesticular islet allografts, as blocking PD-L1 or PD-1, but not PD-

63 islet (NPI) xenografts compared with rhesus islet allografts at 1 hour, 24 hours, and 7 days.

64 reated BALB/c mice acutely rejected C57BL/10 islet allografts at a mean survival time of 13.8 +/- 2.7

65 s with type 1 diabetes mellitus recipient of islet allografts between 1985 and 2006.

66 evidence that HSCs protected cotransplanted islet allografts by exerting comprehensive inhibitory ef

67 these findings indicate that MHC-mismatched islet allografts can be vulnerable to autoimmune pathoge

68 Islet allografts can survive long term in the liver pare

69 treated with CTLA4/Fc acutely rejected their islet allograft, comparable to untreated control animals

70 induced diabetes showed delayed rejection of islet allografts compared with wild type (WT) mice (p <

71 Wild-type hosts uniformly rejected islet allografts, concomitant with the appearance of CD8

72 Islet allografts cultured for three days in bioreactors

73 All pancreatic islet allografts demonstrated the ability to respond to

74 t of the treatments successful in preventing islet allograft destruction in other nonautoimmune combi

75 m CCR2 naive mice or from CCR2 recipients of islet allografts, display lesser allostimulatory capacit

76 Identification of predictor(s) of islet allograft dysfunction (IGD) might allow for early

77 n subjects with type 1 diabetes mellitus and islet allograft dysfunction requiring exogenous insulin.

78 an vigorously destroy MHC class II-disparate islet allografts established in NOD.scid recipients.

79 fter clinical transplantation contributes to islet allograft failure.

80 ecific CD4 T cells can target MHC-mismatched islet allografts for destruction via the "indirect" (hos

81 latory activity in vivo, can protect a human islet allograft from rejection by suppressing signal tra

82 from the WT B6 recipients compared to DBA/2 islet allografts from c-Rel-/- B6 recipients or B6 islet

83 afts from WT B6 recipients compared to DBA/2 islet allografts from c-Rel-/- B6 recipients or syngenei

84 Islet allografts from donor mice exposed to CO are prote

85 vitro generated MDSC can effectively protect islet allografts from host immune attack.

86 ansplantation with HSCs effectively protects islet allografts from rejection in mice.

87 suppressor cells (MDSC) effectively protect islet allografts from rejection without requirement of i

88 Co-transplanted HSCs effectively protected islet allografts from rejection, forming a multi-layered

89 IFN-gamma to Foxp3 was higher with the DBA/2 islet allografts from the WT B6 recipients compared to D

90 NTES, IP-10, and CXCR3 were highest in DBA/2 islet allografts from WT B6 recipients compared to DBA/2

91 may not be sufficient to maintain long-term islet allograft function in an autoimmune environment.

92 monstrates that severe hyperglycemia impairs islet allograft function in BALB/c and NOD mice and that

93 Stable islet allograft function was associated with increased n

94 Four rhesus monkeys with long-term islet allograft function were studied.

95 2X7R is a novel strategy to induce long-term islet allograft function.

96 vel anti-P2XRs strategy to achieve long-term islet allograft function.

97 The islet allografts functioned for 1 week posttransplant; h

98 d transplanted under the kidney capsule with islet allografts genetically matched or disparate to the

99 ed the presence of donor SOCS-1-Tg islets in islet allografts harvested at 22 days posttransplant, wh

100 ts, and more significantly, such intrathymic islet allografts have been shown to induce recipient tol

101 e present study, we evaluated the outcome of islet allografts implanted either simultaneously or afte

102 he kidney capsule, whereas controls rejected islet allografts in 12 days (p < 0.001), and consistent

103 ody induce long-term (>=1 year) tolerance to islet allografts in 5 of 5 nonsensitized, MHC class I-di

104 Twenty percent of islet allografts in CCR5(-/-) animals without other trea

105 delayed the rejection of allogeneic C57BL/6 islet allografts in diabetic female NOD mice.

106 cells (HSC), achieves long-term survival of islet allografts in mice by way of induction of effector

107 can induce tolerance to heart and pancreatic islet allografts in mouse models, but fail to do so afte

108 K-8 treatment also prolonged the survival of islet allografts in newly diabetic NOD mice.

109 e Edmonton clinical trial on the survival of islet allografts in NOD mice.

110 Lymphangiogenesis occurs in islet allografts in response to inflammation and plays a

111 nucleotides in the induction of tolerance to islet allografts in the liver parenchyma.

112 Survival of islet allografts in treated mice is permanent, but skin

113 rify whether failure of initially successful islet allografts in type 1 diabetes is related: to 1) fa

114 destruction and may increase the efficacy of islet allografts in type 1 diabetes.

115 cells acutely destroy MHC class II-deficient islet allografts in vivo, indicating that autoimmune pat

116 onstrate that P2X1R and P2X7R are induced in islet allograft-infiltrating cells, that only P2X7R is i

117 e we present methods to longitudinally track islet allograft-infiltrating T cells in live mice by end

118 ese data indicate that prevascularization of islet allografts is crucial for their subsequent engraft

119 ite, but strikingly failed to infiltrate the islet allograft itself.

120 posure of an islet donor frequently leads to islet allograft long-term survival and tolerance in reci

121 The mixed chimeras accepted donor islet allografts long term.

122 mice treated with rapamycin also maintained islet allografts long-term.

123 ated CL gene levels may enable prediction of islet allograft loss.

124 approach has utility for prediction of human islet allograft loss.

125 n induced hyperacute rejection of subsequent islet allografts (median survival 1 day) associated with

126 In a murine islet allograft model employing a fully major histocompa

127 In a murine islet allograft model, mIL-15/Fc monotherapy is capable

128 In an islet allograft model, T-bet(-/-) nTreg, but not induced

129 estigated their migration and function in an islet allograft model.

130 phopenia in the challenging nonhuman primate islet allograft model.

131 ucing tolerance in all recipients in a mouse islet allograft model.

132 py or in combination with CTLA4/Fc in murine islet allograft models.

133 -derived CCL2 have been associated with poor islet allograft outcome in patients with type 1 diabetes

134 mory T cell-mediated rejection of pancreatic islet allografts placed either in the testis (a privileg

135 ce and complement C5 deficient mice DBA/2 as islet allograft recipients as well as cobra venom factor

136 ) (NSG) mouse model of T-cell-mediated human islet allograft rejection and developed a therapeutic re

137 strates the important role for CCR2 in early islet allograft rejection and highlights the tissue spec

138 tly, CD4 T cells play a central role both in islet allograft rejection and in autoimmune disease recu

139 t the appropriate timing of ALS treatment of islet allograft rejection and significantly prolong graf

140 We aim to define the role of P2XRs during islet allograft rejection and to establish a novel anti-

141 e that expression of SOCS-1 in islets delays islet allograft rejection but cannot circumvent destruct

142 ntegrin antibody and CS1-peptide may prevent islet allograft rejection by altering either T cell acti

143 rapamycin has the potential to inhibit human islet allograft rejection by expanding CD4(+)FOXP3(+) Tr

144 uced, we tested the specific role of CCR2 in islet allograft rejection by transplanting fully MHC mis

145 f such homing can prevent T cell priming and islet allograft rejection despite normal T and B cell fu

146 ecific chemokines and chemokine receptors in islet allograft rejection has not been fully elucidated.

147 We sought to determine the role of CCR5 in islet allograft rejection in a streptozotocin-induced di

148 blockade nor CD28/CD154 blockade can prevent islet allograft rejection in diabetic NOD mice.

149 These data shed light on the mechanisms of islet allograft rejection in different responder strains

150 the allorecognition and effector pathways of islet allograft rejection in different strains of mice,

151 otent immunoregulatory agent that suppressed islet allograft rejection in humanized NOD/SCID mice.

152 as transgenic expression of Bcl-xL restored islet allograft rejection in IkappaBalphaDeltaN-Tg mice.

153 experimental autoimmune encephalomyelitis or islet allograft rejection in murine models.

154 ented CD4 TFH/GC B cell numbers and hastened islet allograft rejection in naive 12-week old Qa-1 defi

155 We now show that islet allograft rejection is associated with a steady in

156 of immunosuppressive reagents for preventing islet allograft rejection is associated with severe comp

157 We demonstrate that MSCs can prevent islet allograft rejection leading to stable, long-term n

158 The exact mechanisms of islet allograft rejection remain unclear, however.

159 nt protein-1 (MCP-1; CCL2) in vitro and that islet allograft rejection was associated with intragraft

160 Syngeneic islet graft and islet allograft rejection was reduced in NOD and B6 mice

161 t tolerizing therapy, does not prevent acute islet allograft rejection when complement C5 deficient D

162 revealed a role for the purinergic system in islet allograft rejection, and the targeting of P2X7R is

163 sulin requirements are indicators of ongoing islet allograft rejection, but there are no methods to p

164 es correlated with and/or were predictive of islet allograft rejection, defined as a loss of C-peptid

165 (using periodate-oxidized ATP [oATP]) delays islet allograft rejection, reduces the frequency of Th1/

166 Because these immune cells are involved in islet allograft rejection, we hypothesized that transpla

167 nflammation as well as suppresses pancreatic islet allograft rejection.

168 nd rDCs, respectively) during the process of islet allograft rejection.

169 C) B cell numbers in naive mice and hastened islet allograft rejection.

170 al T1-type cytokine response observed during islet allograft rejection.

171 pies to prevent beta-cell destruction during islet allograft rejection.

172 and Fas ligand in peripheral blood precedes islet allograft rejection.

173 ut the contribution of chemokine pathways to islet allograft rejection.

174 nt with each reagent alone failed to prevent islet allograft rejection.

175 vide a clinically useful strategy to prevent islet allograft rejection.

176 rain combination, DST results in accelerated islet allograft rejection.

177 estrating the Th1 immune response leading to islet allograft rejection.

178 ls is a rate-limiting step in the process of islet allograft rejection.

179 RMA1 deficiency prevented T-cell priming and islet allograft rejection.

180 ion (DST), although it failed to alter acute islet allograft rejection.

181 s initiation of inflammation, which leads to islet allograft rejection; islet grafts from TLR4-defici

182 transplantation while IDO overexpression in islet allografts restored their long-term survival induc

183 Tolerance to intratesticular islet allografts spread to skin allografts in the non-pr

184 serum (ALS) on day -7 led to 100% permanent islet allograft survival (>200 days) compared to a mean

185 regimen (n = 5) had significantly prolonged islet allograft survival (204, 190, 216, 56, and >220 da

186 ion delivered by lentiviral vector prolonged islet allograft survival (51.0 +/- 2.9 days) by increasi

187 f 0.3 or 1.0 mg/kg KRP203 produced long-term islet allograft survival (9200 days) in one of five and

188 Prolonged islet allograft survival achieved by blockade of the MCP

189 ody efalizumab (EFA), which permit long-term islet allograft survival and address some of these conce

190 uced permanent, T(reg)-dependent cardiac and islet allograft survival and donor-specific allograft to

191 and rapamycin achieved long-term pancreatic islet allograft survival and donor-specific tolerance in

192 munosuppression can have profound effects on islet allograft survival and implicate the expression of

193 IFN-gamma is not always requisite in islet allograft survival but rather varies according to

194 of this study was to explore prolongation of islet allograft survival by cotransplantation with myelo

195 ckade plus gammac blockade markedly prolongs islet allograft survival compared with the controls.

196 safely and as effectively support long-term islet allograft survival compared with the traditional p

197 blockade alone induced indefinite pancreatic islet allograft survival if anti-IL-7R treatment was sta

198 ly, costimulation blockade induced permanent islet allograft survival in (NOD x C57BL/6)F1 mice but n

199 eated dendritic cells (dexDCs) could prolong islet allograft survival in a full major histocompatibil

200 necarbodiimide (ECDI-SPs) induces indefinite islet allograft survival in a full MHC-mismatched model

201 protocol and produce marked prolongation of islet allograft survival in a preclinical model.

202 eatment leads to significant prolongation of islet allograft survival in allosensitized recipients.

203 TIM-1(+) B cells prolonged islet allograft survival in B-deficient mice, whereas TI

204 ability of costimulation blockade to prolong islet allograft survival in congenic NOD mice bearing in

205 CD20 rituximab (Rituxan) promoted long-term islet allograft survival in cynomolgus macaques maintain

206 preparations, resulted in a prolongation of islet allograft survival in immunocompetent recipients.

207 influence the outcome of T-cell deletion and islet allograft survival in mice treated with costimulat

208 ces humoral tolerance and promotes long-term islet allograft survival in mice.

209 olerance protocols have failed in prolonging islet allograft survival in NOD mice.

210 Islet allograft survival in NOD.B6 Idd3 mice treated wit

211 D28 costimulation-blocker CTLA4Ig) prolonged islet allograft survival in nonhuman primates relative t

212 and asked if this combination would promote islet allograft survival in our primate model.

213 ding MHC class II sharing may provide better islet allograft survival in recipients with autoimmune d

214 latacept and sirolimus successfully prevents islet allograft survival in rhesus monkeys, but inductio

215 iabetes development in NOD mice and prolongs islet allograft survival in rodents; yet the mechanisms

216 oinflammatory B cells and promotes long-term islet allograft survival in such recipients.

217 ns of immunomodulation can lead to prolonged islet allograft survival in the challenging NOD mouse mo

218 present study we tested the hypothesis that islet allograft survival in the diabetic NOD mouse is de

219 First, long-term murine islet allograft survival induced by anti-CD45RB is preve

220 t second hand smoke (SHS) hindered long-term islet allograft survival induced by CD154 costimulatory

221 NOD mice, and in NOD.B6/B10 Idd3 Idd5, mice islet allograft survival is similar to that achieved in

222 Islet allograft survival limits the long-term success of

223 ified, ex vivo expanded human Treg prolonged islet allograft survival resulting in the accumulation o

224 with HSC-induced MDSCs significantly extends islet allograft survival through iNOS-mediated T-cell in

225 ith cyclosporine A, OA further prolonged the islet allograft survival to 34+/-3 days.

226 onor, the islets or the recipient, prolonged islet allograft survival to different extents.

227 s ligand (PD-L1, B7-H1), and prolongation of islet allograft survival was abrogated by anti-PD-L1 mAb

228 After BLyS neutralization, indefinite islet allograft survival was achieved.

229 Islet allograft survival was investigated in streptozoto

230 A significant prolongation of islet allograft survival was noted in CCR2-/- recipients

231 After costimulation blockade, islet allograft survival was prolonged in diabetes-resis

232 Islet allograft survival was prolonged in IkappaBalphaDe

233 vitro, 3A8-based therapy markedly prolonged islet allograft survival without depleting B cells.

234 nor beta cells from transgenic mice prolongs islet allograft survival, confirming the negative role o

235 herapeutic course of rapamycin had long-term islet allograft survival, in contrast to the effect of t

236 herapy further promoted HSC mobilization and islet allograft survival, inducing a robust and transfer

237 reatment with KRP203 significantly prolonged islet allograft survival, whereas additional intragraft

238 -2 for 3 weeks significantly prolonged human islet allograft survival.

239 na ascribed to graft rejection hence prolong islet allograft survival.

240 ntation in the testis significantly prolongs islet allograft survival.

241 s graft-specific immune responses to prolong islet allograft survival.

242 ocked, led to HSC mobilization and prolonged islet allograft survival.

243 reactive CD8 T-cells and exhibited prolonged islet allograft survival.

244 mAb significantly prolonged both cardiac and islet allograft survival.

245 OD mice treated with costimulation prolonged islet allograft survival.

246 ine-based DC-depleting strategies to prolong islet allograft survival.

247 se persistence was associated with long-term islet allograft survival.

248 alone or in combination, moderately prolong islet allograft survival.

249 imulation blockade leads to long-term murine islet allograft survival.

250 jection of skin but only minimally shortened islet allograft survival.

251 prevents anti-CD45RB therapy from prolonging islet allograft survival.

252 ta cells from B7-H4 transgenic mice enhances islet allograft survival.

253 mus was well tolerated and induced long-term islet allograft survival.

254 ion in PD-L1 knockout mice failed to prolong islet allograft survival.

255 inated in the host, approximately 40% of the islet allografts survived.

256 ere found to be higher in CCR2 recipients of islet allografts than in WT recipients.

257 ncreased susceptibility of H-2K(b+) skin and islet allografts to rejection is not based on their abil

258 ing is necessary and sufficient for inducing islet allograft tolerance and is necessary but not suffi

259 d hematopoietic chimerism is associated with islet allograft tolerance and may reverse autoimmunity.

260 Islet allograft tolerance could not be induced in diabet

261 Interestingly, MR1 anti-CD154 induces islet allograft tolerance in the absence of CD40/CD154 p

262 The data demonstrate that 1) NOD mice resist islet allograft tolerance induction; 2) unlike skin allo

263 egion gene(s) is an important determinant of islet allograft tolerance induction; and 4) there may be

264 on; 2) unlike skin allografts, resistance to islet allograft tolerance is a genetically recessive tra

265 C10R4) may inhibit the induction of renal or islet allograft tolerance via a mixed chimerism approach

266 or deletion of CD25(+) T cells in vivo broke islet allograft tolerance.

267 D4CD25 regulatory cells are not critical for islet allograft tolerance.

268 D154 co-stimulatory signals would facilitate islet allograft tolerance.

269 oxP3(+) regulatory T cells (Tregs) to induce islet allograft tolerance.

270 Migration of MDSC was examined in an islet allograft transplant model by tracking the systemi

271 8 and responses to IL-18 in a mouse model of islet allograft transplantation.

272 The mean survival time of BALB/c islet allografts transplanted in streptozotocin-induced

273 BALB/c islet allografts transplanted into CCR5(-/-) (C57BL/6) r

274 In contrast, the majority of islet allografts transplanted into CD103(-/-) hosts surv

275 Finally, islet allografts transplanted intrahepatically in plt mi

276 nificantly accelerate the acute rejection of islet allografts transplanted under the renal capsule, a

277 pression of NKG2A by liver NK1.1(+) cells in islet allograft-transplanted mice is involved in the pro

278 nction is commonly observed in recipients of islet allografts treated with high doses of rapamycin.

279 eived transplants of fresh C57BL/10 (H-2(b)) islet allografts under the kidney capsule and were treat

280 WT or iNOS MDSCs were cotransplanted with islet allografts under the renal capsule of diabetic rec

281 gous HSCs and promotes long-term survival of islet allografts via a PD-L1-mediated mechanism.

282 e results of this analysis, an NHBD isolated islet allograft was performed in a type I diabetic.

283 Consequently, a second same-donor islet allograft was rejected in an accelerated fashion b

284 Permanent acceptance of pancreatic islet allografts was achieved in mice treated with the c

285 in transplantation in long-term acceptors of islet allografts was used to test for the development of

286 While BALB/c islet allografts were acutely rejected in B6 MHC class I

287 Some Balb/c recipients of fresh islet allografts were also treated with a tolerogenic pr

288 f treatment, mice remained normoglycemic and islet allografts were functional for up to 120 treatment

289 was eliminated in only the DST or the graft, islet allografts were rapidly rejected.

290 ost-immune responses initiated by pancreatic islet allografts were readily suppressed by a variety of

291 MDSC mixed with islet allografts were transplanted into diabetic recipie

292 elicited prompt rejection of long-surviving islet allografts, whereas CD103(-/-) CD8 cells were comp

293 4 induced long-term survival of DBA/2 (H-2d) islet allografts, whereas treatment with each reagent al

294 with WT MDSCs markedly prolonged survival of islet allografts, which was associated with reduced infi

295 Treatment of recipients of islet allografts with ingested IFN-alpha doubles the tim

296 Treatment of recipients of islet allografts with prolonged ingested IFN-alpha preve

297 loTregs but not nTregs prolonged survival of islet allografts without any other immunosuppressive the

298 histocompatibility complex (MHC)-mismatched islet allografts without maintenance immunosuppressive t

299 ation of MDSC markedly prolonged survival of islet allografts without requirement of immunosuppressio

300 ion with MDSC (not DC) effectively protected islet allografts without requirement of immunosuppressio