ライフサイエンスコーパス: skin allograft

1 +2 relative transplantation of a C3H (H-2k) skin allograft.

2 the immunologic response to the vascularized skin allograft.

3 tolerant mice subsequently challenged with a skin allograft.

4 nological monitoring of peripheral blood and skin allograft.

5 were adoptively transferred to mice-bearing skin allograft.

6 nodes and are able to infiltrate and reject skin allografts.

7 HSCs and induce donor-specific tolerance to skin allografts.

8 s to reject same donor, but not third-party, skin allografts.

9 CD8-deficient mice can vigorously reject the skin allografts.

10 ransplantation tolerance to fully mismatched skin allografts.

11 at the interface between the wound beds and skin allografts.

12 ion response of naive T cells to established skin allografts.

13 ed immune privilege and survived longer than skin allografts.

14 us rejection and were eliminated faster than skin allografts.

15 lege and have good survival as compared with skin allografts.

16 rneal tissue than when they are expressed in skin allografts.

17 ion of full-thickness, MHC-mismatched rhesus skin allografts.

18 anti-IL-6 IMB almost doubled the survival of skin allografts.

19 r non-donor neonatal porcine or mouse BALB/c skin allografts.

20 nd accepted donor-origin but not third-party skin allografts.

21 n BALB/c (H-2d) recipients of C57BL/6 (H-2b) skin allografts.

22 e tolerance to the more resistant kidney and skin allografts.

23 nocytes mediate the angiogenesis response in skin allografts.

24 nt engraftment of cardiac allografts but not skin allografts.

25 iated with the cell infiltrates in the human skin allografts.

26 onged and even indefinite survival of OVA(+) skin allografts.

27 major histocompatibility complex-mismatched skin allografts.

28 oietic chimerism but it led to rapid loss of skin allografts.

29 eral lymph nodes and subsequently migrate to skin allografts.

30 Foxp3(+) T cells protect full MHC-mismatched skin allografts.

31 elf' and capable of rejecting MHC-mismatched skin allografts.

32 ism, and shortens survival of donor-specific skin allografts.

33 tiation factor 88 promotes the acceptance of skin allografts.

34 readily reject allogeneic cells, but not the skin allografts.

35 ation in muscles that received MT but not in skin allografts.

36 occurs at the onset of tissue destruction of skin allografts.

37 poresponsive CD4 T cells also fail to reject skin allografts.

38 er of tolerance to heart and kidney, but not skin, allografts.

39 After implantation of skin allografts, AAT-treated mice had greater numbers of

40 of these mice challenged with donor-matched skin allografts accept these skin grafts, demonstrating

41 Here, we demonstrate that skin allograft acceptance in mice maintained with clinic

42 pressive regimen, reliably induces permanent skin allograft acceptance in this model.

43 operative LM infection prevented cardiac and skin allograft acceptance induced by anti-CD154 and dono

44 (c) Induction of skin allograft acceptance initially depended on the pres

45 on of DST uniformly results in long-term Ld+ skin-allograft acceptance.

46 In RAG(-/-) recipients of skin allografts adoptively transferred with CD4(+) T cel

47 LPL(-/-) mice showed delayed rejection of skin allografts after release from immunosuppression.

48 Remarkably, skin allografts also were rejected acutely by splenectom

49 A4 and inducible costimulator (ICOS), in the skin allograft and draining lymph nodes compared to endo

50 rejection rates due to the immunogenicity of skin allograft and toxicity linked to high doses of immu

51 By using an adoptive transfer model of skin allograft and using specific Vbeta TCR probes, we d

52 ates with delayed rejection of MHC-disparate skin allografts and an impaired immune response against

53 We orthotopically transplanted mouse tail skin allografts and estimated the numbers of transcripts

54 mice are permissive for the growth of human skin allografts and human peripheral blood mononuclear c

55 cells we sought their presence in tolerated skin allografts and in normal skin.

56 ionally suppressive but failed to migrate to skin allografts and inhibit rejection.

57 ance of primary and secondary donor-specific skin allografts and rejection of third-party grafts.

58 demonstrated the vigorous rejection of human skin allografts and the absence of injury to porcine ski

59 abrogate B6.muMT(-/-) mice rejection of A/J skin allografts and this rejection rendered these recipi

60 r histocompatibility complex (MHC) disparate skin allografts and to test cellular and molecular chang

61 d in the frog Xenopus by antibody depletion, skin allografting, and tumor transplantation.

62 1s play an important role in rejecting human skin allografts, and their local modulation is a promisi

63 s for the difference in survival of islet vs skin allografts are not known.

64 g led to enhanced survival of heart, but not skin, allografts associated with impaired localization o

65 he kidney capsule of NNR allografts, but not skin allografts, at 12 days and beyond implies that NNR

66 The tolerant mice accepted the second donor skin allografts but acutely rejected the third-party gra

67 med mice eliminated accelerated rejection of skin allografts but failed to induce tolerance.

68 nged survival of kidney, islet, cardiac, and skin allografts, but again most animals have eventually

69 treatment could not block acute rejection of skin allografts, but interfered with sensitization for s

70 diabetes, nonetheless resist prolongation of skin allografts by costimulation blockade.

71 e showed in a skin transplant model that the skin allografts contain a subset of antigen-presenting c

72 B6AF1 mice received ALS (days -1 and 2), skin allografts (day 0), and BMC and/or thymus grafts (T

73 long-term survival of highly antigenic donor skin allografts despite the presence of functionally int

74 d deletion in the Mig gene were used as both skin allograft donors and recipients in a class II major

75 pressed by CTLs that infiltrate HY-disparate skin allografts during rejection.

76 ex in recipient livers promotes tolerance to skin allografts, even in animals primed to produce a mem

77 length of TCRs expressed by CTL-infiltrating skin allografts expressing the immunogenic H4 peptide du

78 d IFN-gamma), whereas primarily vascularized skin allografts failed to trigger a significant indirect

79 l effectors of microvascular injury in human skin allografts following adoptive transfer into immunod

80 al, and 40% of the recipients accepted their skin allograft for >100 days.

81 Moreover, when we transplanted skin allografts from stable tolerant chimeras onto synge

82 s, even in animals that had already rejected skin allografts from the same donors.

83 e C57BL/6 allograft donors, and B6.H-2(bm12) skin allografts had a 5-day prolonged survival in B6.Mig

84 The acceptance of skin allografts has historically been among the most cha

85 ADAMTS13 treatment and the impact of NETs on skin allografts, however, remain unexplored.

86 Skin allograft in mice was used as an experimental trans

87 of human Tregs to prevent the rejection of a skin allograft in vivo, highlighting the therapeutic pot

88 regs to regulate immune responses to a human skin allograft in vivo.

89 cells (BMC) effectively induces tolerance to skin allografts in antilymphocyte serum- and rapamycin-t

90 ministration of LPS shortens the survival of skin allografts in mice treated with costimulation block

91 ock tolerance induction to hematopoietic and skin allografts in mice treated with costimulation block

92 reactive T cells, and indefinite survival of skin allografts in mice.

93 induces robust transplantation tolerance to skin allografts in mice.

94 reatment significantly prolonged survival of skin allografts in naive recipients as well as heart all

95 e capacity to induce rejection of HA bearing skin allografts in syngeneic hosts.

96 phocytes up-regulate Foxp3 in mice receiving skin allografts in the absence of any treatment.

97 ls led to significantly delayed rejection of skin allografts in the Balb/C->C57BL/6J model.

98 o intratesticular islet allografts spread to skin allografts in the non-privileged sites.

99 In contrast, nonimmunosuppressed cardiac and skin allografts in the same strain combination are rejec

100 nal in the trafficking of human T cells into skin allografts in vivo in the humanized SCID mouse.

101 CD200 mice with long-term surviving cardiac (skin) allografts in the absence of continued transgene i

102 wild-type mice and accelerated rejection of skin allografts, indicating that regulation of homeostat

103 show that long-term survival of vascularized skin allografts induced by anti-CD40L Abs was associated

104 , or OX40 ligand in this model reduces human skin allograft injury and T cell effector molecule expre

105 A human skin allograft injury model in immunodeficient mice, eng

106 f bone marrow donor-type but not third party skin allografts is achieved in CD117-ADC-conditioned chi

107 demonstrate that the survival of human fetal skin allografts is markedly prolonged compared with that

108 uld be new therapeutic strategies to promote skin allograft longevity and, hence, the survival of pat

109 Enhancing skin allograft longevity lessens the need for new allogr

110 gorously rejected fully MHC-mismatched DBA/2 skin allografts (mean survival time, 12 days; n = 6) com

111 molecules critical to T cell rolling within skin allograft microvasculature during the effector phas

112 onkeys were transplanted with full-thickness skin allografts mismatched at both class I and class II

113 Here we used a mouse skin allograft model and an allogeneic radiation chimera

114 Using a skin allograft model in which transplant acceptance is c

115 several points has been examined in a mouse skin allograft model of this protocol.

116 histocompatibility complex-mismatched murine skin allograft model to study graft survival and mechani

117 To explore this role, we employed a skin allograft model using mice with targeted deletion o

118 Unlike the murine skin allograft model, all grafts were rejected within 11

119 Using a highly immunogenic murine skin allograft model, we found that the absence of both

120 n immune responsiveness was examined using a skin allograft model.

121 To test this hypothesis, we utilized murine skin allograft models to identify and characterize Tfh m

122 tocompatibility complex (MHC)-matched murine skin allografting models that were highly contextual in

123 We previously demonstrated that skin allografts monocolonized with the common human comm

124 vo CD44(+)CD8(+) T cells rejected donor-type skin allografts more rapidly than naive CD8(+) T cells d

125 rolonged survival of fully mismatched BALB/c skin allografts on C57BL/6 recipients, with approximatel

126 uniformly achieves >90-d survival of BALB/c skin allografts on C57BL/6 recipients.

127 directs T cell infiltration into B6.H-2bm12 skin allografts on C57BL/6 recipients.

128 onatal donors prolongs the survival of adult skin allografts on rabbit anti-mouse lymphocyte serum-tr

129 required to achieve prolonged engraftment of skin allograft or tolerance to islet allograft in recipi

130 onal metabolic pathways, and their impact on skin allograft outcome and alloimmunity.

131 ter characterize alloreactivity in naive and skin allograft-primed mice, we used a modified, high-res

132 requirement for regulatory CD4(+) T cells in skin allograft recipients could account for this differe

133 By contrast, B cell depletion exacerbated skin allograft rejection and augmented the proliferation

134 re, we found that regional ES delayed murine skin allograft rejection and promoted long-term allograf

135 The mechanism of skin allograft rejection has been thought to require pre

136 ells have been shown to be involved in acute skin allograft rejection in an ectothermic vertebrate.

137 the efficacy of hu5C8 in preventing primary skin allograft rejection in rhesus monkeys.

138 d are surprisingly potent in mediating acute skin allograft rejection in the absence of any adaptive

139 X40 costimulation is critically important in skin allograft rejection in this model, as blocking the

140 Skin allograft rejection in this system occurred in the

141 ules in vitro and can reduce T cell-mediated skin allograft rejection in vivo.

142 Similarly, in vivo, anti-OX40 prevented skin allograft rejection mediated by CD8+ T cells.

143 blockade of OX40-OX40L interactions prevents skin allograft rejection mediated by either subset of T

144 feration or donor Ag priming, induced prompt skin allograft rejection regardless of CD28/CD154 blocka

145 dy, we used a CD8(+) TCR transgenic model of skin allograft rejection to characterize in vivo activit

146 istant CD4(+)OX40(+) cells failed to mediate skin allograft rejection upon adoptive transferring into

147 KA1010 displayed no significant features of skin allograft rejection upon histological analysis at 7

148 able to abolish the stable MC nor to trigger skin allograft rejection, a hallmark of peripheral, not

149 ositive bacteria by oral gavage, all delayed skin allograft rejection, and reduced alloreactive T cel

150 8/CD154 blockade had no effect in preventing skin allograft rejection.

151 dy, hu5C8, greatly delays the onset of acute skin allograft rejection.

152 ays does not adequately inhibit CD8-mediated skin allograft rejection.

153 CTL-detected peptides primed for accelerated skin allograft rejection.

154 d in a murine model for CD4+ T cell-mediated skin allograft rejection.

155 gs from the OX40(+) cells resulted in prompt skin allograft rejection.

156 vivo cytotoxicity assay and correlated with skin allograft rejection.

157 of CD4+ T cells to reject class I mismatched skin allografts remains controversial.

158 their contribution to the rejection of human skin allografts remains unknown.

159 The use of skin allografts represents a lifesaving strategy for sev

160 let allograft tolerance induction; 2) unlike skin allografts, resistance to islet allograft tolerance

161 to transplantation of a fully MHC mismatched skin allograft resulted in prolonged allograft survival.

162 Re-exposure of C57BL/6 mice to HLA.A2(+) skin allografts resulted in a surge of donor-specific (a

163 n by Treg that simultaneously infiltrate the skin allografts, resulting in a failure to generate dono

164 ty in mice that rejected fully MHC-disparate skin allografts revealed a high frequency of interferon

165 vitro data, analysis of lymph nodes draining skin allografts revealed that OX40 blockade had no effec

166 NZW H2(z); or BALB/c H2(d)) heart, aorta, or skin allograft significantly compared with treatment wit

167 act hypersensitivity responses and tolerated skin allografts significantly longer than wild-type mice

168 allografts were unable to reject B6.H-2bm12 skin allografts, suggesting potential down-regulatory me

169 n with CD28/CD154 blockade induced long term skin allograft survival (>100 days; n = 5).

170 SC4 was also able to significantly prolong skin allograft survival across a MHC class I barrier.

171 arrow-cell (BMC) infusion induces indefinite skin allograft survival across fully mismatched mouse st

172 (3) Skin allograft survival after adoptive transfer of MDSCs

173 dents demonstrated prolongation of heart and skin allograft survival after peptide therapy.

174 Notably, the most pronounced extension of skin allograft survival and attenuation of alloimmunity

175 e of localized immune delivery in prolonging skin allograft survival and its potential utility in tre

176 yte serum (ALS) and sirolimus (Sir) prolongs skin allograft survival and produces chimerism.

177 Previous studies have shown that skin allograft survival can be augmented by the administ

178 ection sensitive to rapamycin, and long term skin allograft survival can be readily induced by rapamy

179 Costimulation blockade fails to prolong skin allograft survival in (NOD x C57BL/6)F1 mice and in

180 iciency of IL-2 complex (cplx) treatment for skin allograft survival in a stringent murine skin graft

181 latory activity in vivo, promoting long-term skin allograft survival in a stringent transplantation m

182 n of sirolimus (rapamycin) to induce maximal skin allograft survival in ALS-treated, BM-infused recip

183 atment with DST and anti-CD154 mAb prolonged skin allograft survival in both C57BL/6 (H2b) and C57BL/

184 costimulatory pathways effectively promotes skin allograft survival in C3H/HeJ mice, extending media

185 BL, or CD27/CD70 pathway, markedly prolonged skin allograft survival in CD28/CD154 DKO mice.

186 ive growth factor signals produced long term skin allograft survival in CD4-deficient mice (mean surv

187 locking OX40 costimulation induced long term skin allograft survival in CD4-deficient mice and CD8-de

188 affinity IL-2R, CD25, and IL-2 in prolonging skin allograft survival in mice receiving combined CD40/

189 c transfusion (DST) of spleen cells prolongs skin allograft survival in mice through a mechanism invo

190 are more potent than whole BM at prolonging skin allograft survival in mice treated with ALS and Sir

191 on of transplantation tolerance and shortens skin allograft survival in mice treated with costimulati

192 (mAb) induces permanent islet and prolonged skin allograft survival in mice.

193 ibody leads to permanent islet and prolonged skin allograft survival in mice.

194 thways has been shown to effectively promote skin allograft survival in mice.

195 herapy resulted in prolongation of heart and skin allograft survival in mice.

196 cross-decoration of leukocytes and prolongs skin allograft survival in mice.

197 longed minor-mismatched and major-mismatched skin allograft survival in mice.

198 154 mAb plus DST treatment failed to prolong skin allograft survival in nondiabetic male NOD mice.

199 as been reported to induce long-term primary skin allograft survival in primates.

200 cells, or buffy coat cells led to prolonged skin allograft survival in recipients treated with anti-

201 node cells, or buffy coat cells can prolong skin allograft survival in recipients treated with costi

202 pon adoptive transfer, significantly prolong skin allograft survival in vivo.

203 treatment, and under such conditions stable skin allograft survival is difficult to achieve.

204 Induction of skin allograft survival requires the presence of CD4 cel

205 de enjoy a significantly greater increase in skin allograft survival than do wild-type mice.

206 Costimulation blockade prolonged skin allograft survival that was shortened after coinjec

207 Skin allograft survival was also prolonged in normal rec

208 Skin allograft survival was correlated with the recipien

209 Skin allograft survival was monitored, and the prolifera

210 al Tregs, a synergistic effect in prolonging skin allograft survival was observed.

211 Skin allograft survival was prolonged for up to 17.8+/-0

212 L/6 congenic mice with NOD-derived Idd loci, skin allograft survival was readily prolonged by costimu

213 ation blockade plus LPS also exhibited short skin allograft survival whereas similarly treated B6.CD8

214 CD4CD25 cells are required for induction of skin allograft survival, (2) CD4CD25 T cells are not req

215 We examined long-term cardiac and skin allograft survival, alloantigen-induced T-cell prol

216 n with CD28/CD154 blockade induced long-term skin allograft survival, and 40% of the recipients accep

217 X40 ligand pathway alone did not prolong the skin allograft survival, but blocking OX40 costimulation

218 al antibody (mAb) markedly prolongs heart or skin allograft survival, but the influence of this strat

219 a diverse microbiota significantly prolonged skin allograft survival, identifying a probiotic with th

220 n of alloreactive CD8+ T cells and shortened skin allograft survival.

221 5 cell deletion had no effect upon healed-in skin allograft survival.

222 deplete, peripheral chimerism and maintained skin allograft survival.

223 CD8(+) T cells and was associated with brief skin allograft survival.

224 es, costimulation blockade failed to prolong skin allograft survival.

225 s necessary but not sufficient for long-term skin allograft survival.

226 IDEC-131 modestly prolongs rhesus skin allograft survival.

227 and the gamma(c) pathways induced prolonged skin allograft survival.

228 ALS induces prolonged cardiac and second-set skin allograft survival.

229 row or donor splenocytes results in extended skin allograft survival.

230 allografts and dramatically prolongs primary skin allograft survival.

231 induce a significant prolongation in BALB/c skin allograft survival.

232 ession, resulting in significantly prolonged skin allograft survival.

233 mediated T cell depletion markedly prolonged skin allograft survival.

234 utoimmune encephalitis and enabled long-term skin allograft survival.

235 c anti-IL-6 receptor treatment in prolonging skin allograft survival.

236 costimulatory molecules, and prolongation of skin allograft survival.

237 e of donor but not recipient MCP-1 prolonged skin allograft survival.

238 BN skin allografts survived significantly longer on protein

239 A skin allograft system was used to demonstrate that disse

240 mmune responses to microbial antigens and to skin allografts, the prevailing view has been that the i

241 ombined immunodeficiency recipients of B10.A skin allografts, this cell line specifically induced a f

242 class I can enhance tolerance to subsequent skin allografts through indirectly expanded nTreg leadin

243 tion of thymectomy to the protocol permitted skin allografts to survive for > 100 d, suggesting that

244 a donor-specific transfusion or DST) permits skin allografts to survive for >100 days in thymectomize

245 rable mixed chimerism is required for murine skin allograft tolerance (TOL), renal allograft TOL has

246 etic basis for the resistance of NOD mice to skin allograft tolerance also applies to islet allograft

247 e hematopoietic chimerism and donor-specific skin allograft tolerance and justify further development

248 s study, we demonstrate that a stable MC and skin allograft tolerance can be established across MHC b

249 engraftment and induction of donor-specific skin allograft tolerance has recently been described.

250 ogeneic bone marrow engraftment and specific skin allograft tolerance induction.

251 of alloreactive T cells and produced stable skin allograft tolerance, a very stringent test of allog

252 In models of skin allograft tolerance, tumor growth, and experimental

253 ment increased durable donor-specific BALB/c skin allograft tolerance.

254 has been studied in several models including skin allograft tolerance.

255 Here, we demonstrate a dominant skin-allograft tolerance model induced by a single DST a

256 We studied the survival of skin allografts transplanted from fully allogeneic (BALB

257 stocompatibility complex disparate heart and skin allografts transplanted into CD8 knockout recipient

258 allowed permanent survival of heart, but not skin, allografts transplanted across a major histocompat

259 In the skin allograft, Tregs increased after low-dose IL-2 ther

260 1l) to Buffalo (RT1b) rat cardiac, renal, or skin allograft was studied.

261 Tolerance to fully MHC-incompatible skin allografts was induced as follows: C57Bl/10 (H2b) r

262 Modest prolongation of skin allografts was observed in mice reconstituted with

263 the associated angiogenesis reactions in the skin allografts were analyzed temporally by videomicrosc

264 unity, mice given costimulation blockade and skin allografts were coinjected with TLR2 (Pam3Cys), TLR

265 wever, after cessation of anti-OX40 therapy, skin allografts were eventually rejected indicating that

266 phate buffered saline-treated animals, human skin allografts were infiltrated with lymphocytes and de

267 rafts survived long term (>84 days), whereas skin allografts were rapidly rejected ( approximately 13

268 BALB/c skin allografts were transplanted onto C57BL/6 Rag 1-/-

269 C57BL/6 recipients of BALB/c skin allografts were treated with DSBM (150 x 10(6) cell

270 Full-thickness skin allografts were used in C3H to B6AF1 (class I misma

271 ces specific unresponsiveness (tolerance) to skin allografts, which can be augmented by the adjuvant

272 proliferative response in vivo to heart and skin allografts, which in both cases was localized to re

273 ion, in contrast to that seen in response to skin allografts, which was delayed until 10-12 days afte

274 ating gene(-/-) mice, which received an H2b+ skin allograft with and without anti-OX40.

275 guingly, sorafenib prolonged the survival of skin allograft without major toxicity.

276 r-specific BM induced tolerance to renal and skin allografts without inducing hematopoietic chimerism

277 f major histocompatibility complex-different skin allografts without the need for immunosuppression.

278 nontolerant lymphocytes from rejecting fresh skin allografts, without hindrance of rejection of third