ライフサイエンスコーパス: skin graft

1 hepatocytes 7 days before challenge with a K skin graft.

2 moval of necrotic tissues covered by a split-skin graft.

3 e of donor skin and rejection of third-party skin graft.

4 ific CD8(+) T cells were more abundant after skin graft.

5 ction after challenge with an OVA-expressing skin graft.

6 uces a rapid destruction of the transplanted skin graft.

7 nstruction using a temporary split-thickness skin graft.

8 nely closed with a Vicryl mesh followed by a skin graft.

9 al blood mononuclear cells allogeneic to the skin graft.

10 g the CD8 T cell memory response to a second skin graft.

11 I on recipient DCs during the life span of a skin graft.

12 and cardiac transplants but not conventional skin grafts.

13 mice rejected MHC mismatched murine C57BL/6J skin grafts.

14 arget antigen and to rejection of autologous skin grafts.

15 e could be prevented by simultaneous class I skin grafts.

16 nance was observed in primarily vascularized skin grafts.

17 ve transfer of Ab to SCID mice bearing human skin grafts.

18 in WF recipients after rejection of the ACI skin grafts.

19 and effector function of TCR-tg T cells than skin grafts.

20 lerated rejection of minor H-locus disparate skin grafts.

21 ocus allele (class II) identical third-party skin grafts.

22 nts subsequently received donor-strain MT or skin grafts.

23 female on B6 background) antigen-mismatched skin grafts.

24 s tested using mixed lymphocyte cultures and skin grafts.

25 allograft survival accepted ACI but not PVG skin grafts.

26 e mice that had been transplanted with human skin grafts.

27 orrelated with the involution and loss of Tg skin grafts.

28 two of four animals rejecting delayed donor skin grafts.

29 tivated exocytosis and inflammation in human skin grafts.

30 ly are able to effectively reject allogeneic skin grafts.

31 e marrow permanently accepted K(b) disparate skin grafts.

32 sfer into syngeneic Balb/c hosts bearing HA+ skin grafts.

33 of fibroblasts and keratinocytes in cultured skin grafts.

34 modulation led to permanent acceptance of F1 skin grafts.

35 and prevent normal pigmentation of resulting skin grafts.

36 kin grafts and promptly rejected third-party skin grafts.

37 nor (bm1 or F1) and third-party B10.BR (H-2) skin grafts.

38 olonged survival of minor antigen-mismatched skin grafts.

39 vely, one of them after receiving additional skin grafts.

40 d delayed rejection of subsequent donor-type skin grafts.

41 ficant reduction of mutant Krt75 mRNA in the skin grafts.

42 Four patients (two in each study group) had skin grafts.

43 ere given donor, third-party, and autologous skin grafts.

44 graft and promptly rejected the third-party skin grafts.

45 ) T cells and subsequently the acceptance of skin grafts.

46 nor acceleration of rejection of allogeneic skin grafts.

47 fter simultaneous peptide administration and skin grafting.

48 lass I-disparate bm1 mice 7 d prior to donor skin grafting.

49 Donor-specific tolerance was tested by skin grafting.

50 afts, although incomplete tolerance to donor skin grafting.

51 burn excision and autologous split-thickness skin grafting.

52 well as secondary wound closure by means of skin grafting.

53 s, and then repair with advancement flaps or skin grafting.

54 ignificantly accelerated rejection of OVA(+) skin grafted 7 days after hepatocyte transplantation.

55 imal doses of tacrolimus to induce long-term skin graft acceptance in this stringent transplant model

56 2 deficiency and led to long-term allogeneic skin graft acceptance.

57 which supports a regulatory role for LCs in skin graft acceptance.

58 endothelial cells (EC) in vascularized human skin grafts allogeneic to the T cell donor.

59 rAAV-K-treated B10.BR animals primed with K skin grafts also accepted secondary K skin grafts in the

60 group 1 animals were tolerant to their donor skin graft and promptly rejected the third-party skin gr

61 ative for this reactivity was immunized by a skin graft and subcutaneous injections of peripheral blo

62 h broad clinical implications for allogeneic skin grafting and sepsis.

63 myeloablative regimen were tolerant to donor skin grafts and both primary and secondary donor MT (>90

64 w that antigen-specific Tregs induce, within skin grafts and dendritic cells, the expression of enzym

65 prior priming with allogeneic splenocytes or skin grafts and exhibited features of memory as it could

66 indirect alloresponse against MHC-mismatched skin grafts and hence the generation of IgG alloantibodi

67 n 10, and PD-1 (and PD-L1/PD-L2) in tolerant skin grafts and increased expression of mRNAs for indole

68 evidenced by the acceptance of second donor skin grafts and loss of circulating donor-specific Abs.

69 were challenged with simultaneous donor-type skin grafts and peptide.

70 The chimeras accepted donor skin grafts and promptly rejected third-party skin graft

71 In addition, using skin grafts and skin reconstitution assays we demonstrat

72 Currently available skin grafts and skin substitutes for healing following t

73 glutamate is increased in mice that receive skin grafts and that mice treated with glutamate recepto

74 s the rejection of secondary donor-type test skin grafts and to inhibit alloreactive CD8(+) T cell ac

75 ic (H-2d) cardiac grafts and secondary donor skin grafts, and that splenocytes from these tolerant mi

76 the primary graft, three with donor-matched skin grafts, and two with donor class-I peptides to elim

77 al lymphoid organs rejected H-Y incompatible skin grafts as rapidly as wild type mice and exhibited n

78 esis, JH(-/-) mice rejected H-Y-incompatible skin grafts as rapidly as wild-type mice.

79 Mixed lymphocyte reaction (MLR) and skin grafting assessed donor-specific tolerance in vitro

80 r histocompatibility complex (MHC) disparate skin grafts at the peak of acute rejection (seven days p

81 ficient (BKO) mice (B6) were challenged with skin grafts (B/c).

82 If heart transplants are preceded by skin grafts bearing both H60 and HY incompatibilities to

83 we describe bone marrow transplantation and skin grafting between WT and KO mice to assess the contr

84 blockade accelerated MHC class II-mismatched skin graft (bm12 (I-Abm12) into B6 (I-Ab)) rejection in

85 edly prolonged compared with split-thickness skin grafts but not indefinite.

86 transplantation tolerance to OVA-expressing skin grafts, but Foxp3-independent tolerance when the Ag

87 transferred allogeneic Tregs and allogeneic skin grafts, but tolerance to such allografts that lacke

88 bly and predictably reject a xenogenic mouse skin graft by a human T cell mediated mechanism.

89 t rejected donor MHC-matched split-thickness skin grafts by day 25, without changes in renal graft fu

90 ol, were always able to prevent rejection of skin grafts by naive CD4(+) T cells, and did so with no

91 Acceptors of VCA were tolerant of a donor skin graft challenge and no anti-donor antibodies were d

92 Long-term acceptors were tolerant to a donor skin graft challenge even in the absence of peripheral b

93 short-term CD4 blockade at the time of first skin graft challenge only delayed alloreactive CD8 activ

94 LPS infusion in conjunction with donor-type skin graft challenge, failed to break Treg-mediated immu

95 MLR and skin grafting confirmed donor-specific tolerance in euth

96 These data suggest that GalT-KO skin grafts could provide an early first-line treatment

97 h donor-matched skin allografts accept these skin grafts, demonstrating progression to "true" toleran

98 Animals challenged with donor skin grafts displayed prolonged graft survival without p

99 ed kidneys leads to sensitization, but donor skin grafts do not.

100 k wave therapy (ESWT) can enhance healing of skin graft donor sites, this study focused on shock wave

101 the splenocytes from mice which had rejected skin grafts (effector/memory response).

102 In contrast, skin grafts elicited both direct and indirect CD4+ T-cel

103 bred strain CBA do not reject syngeneic male skin grafts even though they mount a T-cell response aga

104 poq-Cre(tg/+)Pparg(fl/fl) mice, coupled with skin graft experiments, showed that the early defects ob

105 Skin grafting experiments confirmed the stratum corneum

106 Adoptive transfer and skin grafting experiments were conducted to assess wheth

107 n adhesion strength compared with staples in skin graft fixation, and removal force of ~4.5 N cm(-2)

108 ouse system, we transplanted mice with human skin grafts followed by allogeneic populations of PBMCs

109 Full-thickness skin grafts followed more than 100 days posttransplantat

110 d as newborns with human HSCs rejected human skin grafts from a histoincompatible donor, indicating t

111 m the hindlimb donor strain and rejection of skin grafts from a third-party donor strain.

112 study from this laboratory demonstrated that skin grafts from alpha-1,3 galactosyltransferase knockou

113 Skin grafts from animals with different AIB1 genotypes a

114 B6 hosts acutely rejected skin grafts from B6.C.H-2 (bm1) and F1 (B6 x bm1) mice.

115 Simultaneously, fully allogeneic skin grafts from BALB/c donors were performed.

116 Skin grafts from BALB/C mice were transplanted into C57B

117 Further, skin grafts from donor, host, and third party showed goo

118 ll KA274 reconstituted C57BL/6 mice accepted skin grafts from HLA-A2.1 transgenic mice for more than

119 ensitized eight macaques with two sequential skin grafts from MHC-mismatched donors; four of them wer

120 Skin grafts from mice expressing human bullous pemphigoi

121 Here, we develop skin grafts from mouse and human epidermal progenitors t

122 ould also be prevented locally by implanting skin grafts from normal mice onto the backs of EPP recip

123 h HY-specific Tregs protected syngeneic male skin grafts from rejection by immune-competent recipient

124 c TCR-transgenic CD4+ T cells protected male skin grafts from rejection by syngeneic females.

125 Previously frozen skin grafts from the bone marrow donor were placed on th

126 Split thickness skin grafts from the hematopoietic cell donor swine were

127 ats, as evidenced by acceptance of secondary skin grafts from the hindlimb donor strain and rejection

128 layed donor-specific tolerance also accepted skin grafts from the same, but not a third-party, donor

129 minor histocompatibility Ag (HY)-mismatched skin grafts from TORC2(DC-/-) donors into wild-type reci

130 a role for TSP1 in regulating full thickness skin graft (FTSG) survival.

131 Also, skin grafts (H-2b) were placed onto SCID mice (H-2d) tha

132 d the survival of Flt3L(-)/(-) heart or tail skin grafts (H2(b)) in allogeneic wt (BALB/c; H2(d)) rec

133 st reported case of orf virus infection in a skin graft harvest.

134 rn patient who developed skin lesions on her skin-graft harvest and skin-graft recipient (burn) sites

135 lerance does not extend universally to donor skin grafts, however, with two of four animals rejecting

136 In human skin grafts implanted on immunodeficient mice, administr

137 did not reject the corresponding allogeneic skin graft in secondary Scid recipients.

138 A streamlined method of skin grafting in mice is described.

139 han 245 days but rejected third-party Balb/c skin grafts in 12 days.

140 Although donor-matched skin grafts in animals tolerant to kidneys induced antid

141 ed survival comparable to that of allogeneic skin grafts in baboons.

142 However, HC donor-derived skin grafts in four recipients with MC developed an infl

143 ly T-cell-mediated rejection of transplanted skin grafts in mice via the release of a proteolytically

144 e survival of DLA-identical HC donor-derived skin grafts in recipients with MC compared to normal rec

145 Th17 cell lines could inflict on allogeneic skin grafts in the absence of other adaptive lymphocytes

146 with K skin grafts also accepted secondary K skin grafts in the long term (MST>100 days) compared to

147 afts, even in recipients that had accepted K skin grafts in the long term.

148 ily vascularized cardiac allografts mimicked skin grafts in the observed immunodominance, and H60 imm

149 ed in long-term Treg-dependent acceptance of skin grafts in the setting of innate immune signals that

150 n all nine of the surviving HC donor-derived skin grafts in this group, but there was no graft loss a

151 contrast, rejection of ovalbumin transgenic skin grafts in TORC2(DC-/-) recipients was unaffected.

152 nor histocompatibility (H) antigen-disparate skin grafts in vivo and induces MHC-restricted CTL respo

153 lls did not result in toxicity against human skin grafts in vivo.

154 CD28 accelerated the rejection of allogeneic skin grafts in young RAG2(-/-) recipient mice.

155 mals led to fulminant rejection of heart and skin grafts, in contrast to grafts on group 2 animals th

156 tantially improve healing quality and reduce skin grafting incidents and thus pave the way for clinic

157 monstrated that IL-17 in HPV16 E7 transgenic skin grafts inhibited effective host immune responses ag

158 ody provide a model optimized for both human skin graft integrity and engraftment of a functional hum

159 In contrast, human skin graft integrity is excellent on CB17-scid bg (SCID.

160 engraft with human immune systems, but human skin graft integrity is poor.

161 f the nail unit followed by a full-thickness skin graft is a safe and efficient treatment for SUSCC w

162 ecific pigmentation in reconstructs used for skin grafting is incompletely understood.

163 Obtaining pigmentary function in autologous skin grafts is a current challenge for burn surgeons as

164 CD4, CD25CD4, and PerforinCD8 cells, whereas skin grafts lacked infiltration.

165 We report that rejection of primary GalT-KO skin grafts led to an anti-xenogeneic humoral response w

166 C developed an inflammatory reaction without skin graft loss.

167 These data suggest that skin grafts may actually augment rather than abrogate do

168 In a model of stable MC, DST to skin grafts may be complete or partial.

169 Local, random-pattern flaps and skin grafts may be inadequate because of the hand's fini

170 A human-murine chimeric skin graft model constructed with KID-KCs mimicked patie

171 We next performed skin graft model to testify the role of sorafenib-induce

172 an survival time in the fully MHC-mismatched skin graft model using this protocol is more than 100 da

173 kin allograft survival in a stringent murine skin graft model.

174 morphology was investigated using an in vivo skin graft model.

175 duce AD-like skin architecture in an in vivo skin graft model.

176 cells into malignancy in a regenerated human skin grafting model.

177 Using a skin-grafting model, we demonstrated that IL-17 in HPV16

178 lation (n = 2), local skin flaps (n = 3), or skin grafts (n = 3).

179 Rag(-/-) skin graft recipients, resulted in skin graft necrosis in all recipients; the generation an

180 ltrate and no chronic rejection in the donor skin grafts of BCNU treated mice compared no BCNU treate

181 Human skin grafts of control mice and normal mouse skin on the

182 demonstrated by the long term acceptance of skin grafts of donor but not third party origin.

183 ere defective in rejecting Balb/C allogeneic skin grafts on C57BL6/J recipients.

184 Skin grafts on group 3 and group 4 animals led to fulmin

185 Tg skin grafts on Wt mice developed neutrophil-rich infiltr

186 in resident in the skin when transplanted by skin graft onto naive mice.

187 and two normal sera were injected into human skin grafted onto athymic, nude mice.

188 KO skin grafted onto either WT or KO animals showed a sixfo

189 Examination of wild-type skin grafted onto Fgfbp1 GFP-knock-in reporter hosts and

190 Sebaceous glands in Fatp4 null skin grafted onto nude mice were found to be dystrophic

191 Transplantation of B6.Mig(-/-) skin grafts onto B6.H-2(bm12).Mig(-/-) recipients result

192 orary coverage with allogeneic human cadaver skin grafts or synthetic skin substitutes.

193 participants whose treatment had failed, had skin grafting, or were coinfected with human immunodefic

194 ed with prolonged survival of the subsequent skin graft (P=0.02).

195 However, less than 50% of skin grafts persist beyond 25 days.

196 Here, we tested the hypothesis that skin grafts prevent rejection after simultaneous peptide

197 r CD200 BL/6 recipients of BALB/c cardiac or skin grafts received low-dose rapamycin (0.5 mg/kg) at 3

198 elevated plaques were observed in all human skin grafts receiving BP IgE (n=11), but not control IgE

199 ance was not observed because donor-specific skin graft rechallenge in nonrejecting animals resulted

200 d skin lesions on her skin-graft harvest and skin-graft recipient (burn) sites.

201 Skin graft recipients with exposures to animals may be a

202 B(high)CD4(+) effector T cells into Rag(-/-) skin graft recipients, resulted in skin graft necrosis i

203 eactive CD4(+) T cells were transferred into skin graft recipients, we observed that a critical CD4(+

204 Adoptively transferred TEa cells in skin-graft recipients were not exhausted.

205 of the nail unit followed by full-thickness skin graft reconstruction from January 1, 2000, to Augus

206 xcision of the nail unit with full-thickness skin graft reconstruction on a series of patients with S

207 tion and increased apoptosis in vitro and in skin grafts regenerated on mice, which was correlated wi

208 MHC genes would explain why cheetahs ablate skin graft rejection among unrelated individuals.

209 plore the involvement of Langerhans cells in skin graft rejection and describe fascinating results.

210 H60 incompatibility does not result in skin graft rejection and only a minority of heart transp

211 no inhibition or even acceleration of donor skin graft rejection compared with non-DST control (naiv

212 od subtly yet reproducibly decreases time to skin graft rejection elicited by central but not effecto

213 days postburn results in enhanced allogeneic skin graft rejection in unburned recipient mice.

214 drug-modified DCs prior to transplantation, skin graft rejection kinetics were similar to those in n

215 diac rejection, chronic renal rejection, and skin graft rejection were compared using CD20 or CD19 mA

216 pecific Treg cells significantly delayed CBK skin graft rejection without any other immunosuppression

217 ates that subsequent to T cell initiation of skin graft rejection, platelets contribute to further T

218 administered systemically in mouse models of skin graft rejection, these nanosensors preferentially a

219 umab (anti-CD3 mAb) and found it could delay skin graft rejection, whereas ipilimumab (anti-CTLA-4 [c

220 d to the CD8+ T effector cells requisite for skin graft rejection.

221 ry mediators and accelerate T cell-meditated skin graft rejection.

222 pairs both CD8 T cell infiltration and acute skin graft rejection.

223 nting CBK but not third-party B10.A (H2k+Dd) skin graft rejection.

224 - T cells, however, had no influence on male skin graft rejection.

225 G-Neutrophils, were confirmed by third-party skin graft rejection; importantly, a graft-versus-leukem

226 le chimeric transplants, preserved antidonor skin graft responses, and normal serum creatinine levels

227 at presensitization of recipients with donor skin grafts results in rejection of subsequent renal all

228 model of fulminant meningococcemia in human skin grafted SCID mice using the wild-type strain 2C4.3.

229 was not permissive for linked suppression to skin grafts sharing donor and third-party alloantigens,

230 Specific tolerance is observed to pig skin grafts sharing the THY donor MHC.

231 ant rejection, whereas haptoglobin-deficient skin grafts showed delayed acute rejection and antidonor

232 Compared to MHC-disparate skin grafts, skin differing from the host only by minor

233 We report a new skin-grafting strategy that stabilizes the Li metal-liqu

234 rogeny of bone marrow SP cells and prolonged skin graft survival across this class I MHC barrier unti

235 Skin graft survival and healing requires rapid restorati

236 e that adoptive transfer of B cells prolongs skin graft survival but only when the B cells were isola

237 en proven in an islet transplantation model, skin graft survival could not be prolonged.

238 Skin graft survival on high CD47 recipients was prolonge

239 ctive T cell frequencies exhibited long-term skin graft survival upon CD28/CD154 blockade, whereas si

240 However, prolongation of skin graft survival was lost when B cells were isolated

241 anti-CD40L blockade plus drug-modified DCs, skin graft survival was prolonged, suggesting endogenous

242 Skin graft survival was unaffected.

243 ntibody production and resulted in prolonged skin graft survival, suggesting the induction of both T-

244 ng both allogeneic bone marrow chimerism and skin graft survival, whereas 7E1-G1 was not.

245 autoimmune colitis, and prolongs allogeneic skin graft survival.

246 with indirect alloresponse further prolonged skin graft survival.

247 evelopment of diabetes, chimerism, and donor skin graft survival.

248 oresponse, we were able to induce indefinite skin graft survival.

249 TSP1 through CD47 limits skin graft survival.

250 lls at the time of transplantation prolonged skin graft survival.

251 ect on the rejection of skin, CXCR3-/- donor skin grafts survived significantly longer than WT contro

252 We investigated whether donor CD200 BL/6 skin grafts taken from primary control or CD200 recipien

253 nsferred into lymphopenic recipients of male skin grafts, Th17 lines elicited a damaging reaction wit

254 that can prevent rejection of donor-specific skin grafts that are mediated by naive CD45RB(high)CD4(+

255 rejection of the first MHC class I disparate skin graft, the suppressive environment was maintained,

256 etion in CBA mice that received CBK (H2k+Kb) skin grafts, the expanded Treg cells preferentially accu

257 Remarkably, when such animals were skin grafted, they exhibited dominant tolerance to those

258 in penile reconstruction are glansectomy and skin grafting to fashion a neoglans in penile cancer and

259 formed only small skin tumors in orthotopic skin grafts to CXCR2 intact hosts, whereas transformed w

260 se against sequential GalT-KO and allogeneic skin grafts to determine whether such serial grafts coul

261 the skin are generated by introducing human skin grafts to immunocompromised rodent strains.

262 Mixed chimerism and skin graft tolerance were achieved in NOD mice receiving

263 nTreg) and depletion of Foxp3 Treg abrogates skin-graft tolerance.

264 antigen-bearing host is also confirmed in a skin graft transplantation model.

265 Mechanical stimulation of DM skin or DM skin graft transplanted onto the WT host resulted in red

266 cells injected under full-thickness COL-EGFP skin grafts transplanted in nonreporter mice developed i

267 Human skin grafts transplanted onto immunodeficient NSG, SCID.

268 indefinitely, prolongs the survival of male skin graft transplants in an Ag-specific manner.

269 have been used in the field of medicine for skin grafts, treatment of burns, and ulcerated skin cond

270 have been used in the field of medicine for skin grafts, treatment of burns, ulcerated skin conditio

271 i.d. injection, these mice reliably develop skin graft-versus-host disease (GVHD) by day 7.

272 ells had a significantly higher incidence of skin graft-versus-host disease compared with mice receiv

273 toxicity was observed, except for a grade II skin graft-versus-host disease in the patient treated fo

274 icity in eight patients (38%), grade 1 acute skin graft-versus-host disease in two patients (10%), an

275 Two patients had episodes of skin graft-versus-host disease that responded to steroid

276 One patient developed grade I skin graft-versus-host disease.

277 been replaced by donor cells, exhibit marked skin graft-vs-host disease, demonstrating that LC can tr

278 nged compared to normal recipients even when skin grafting was delayed until after rejection of the H

279 Survival of DLA-identical HC donor-derived skin grafts was also significantly prolonged compared to

280 after nonmyeloablative conditioning, DST to skin grafts was evaluated in dog leukocyte antigen (DLA)

281 In murine models of MHC mismatched skin grafting, we investigated whether it is feasible to

282 recipients primed with a H-2K-expressing (K) skin graft were injected with rAAV-expressing H-2K (rAAV

283 Healed skin grafts were also noted.

284 In both combinations, skin grafts were also rejected.

285 Skin grafts were placed distal to the popliteal fossa an

286 Skin grafts were placed on group 4 animals, on one group

287 Furthermore, second donor-type skin grafts were rejected and provoked rejection of the

288 Allogeneic skin grafts were rejected by recipients treated with ant

289 Although D2 skin grafts were rejected with a median survival time of

290 dvantage was lost when vascularized CXCR3-/- skin grafts were used as donors in the SCID model of rej

291 matched but minor antigen-mismatched tissue (skin) grafts were transplanted into MHC-heterozygous rec

292 marrow prevented rejection of K(b) disparate skin grafts when adoptively transferred into immunodefic

293 emory CD4 T cells lose the ability to reject skin grafts when transiently placed in an environment in

294 geneic PBMCs alone consistently reject human skin grafts, whereas those also receiving Tregs display

295 rAAV-K-treated B10.BR mice accepted K skin grafts with increased median survival time (MST) mo

296 (BL/6 WT) or CD200(tg) mice received BALB/c skin grafts with rapamycin (1 mg/kg/36 hr) for 7 days.

297 Flt3L(-)/(-) mice rejected BALB/c heart or skin grafts with similar kinetics as B6 wt recipients.

298 MR1-treated mice also accepted a second Tg skin graft without durable production of hBPAG2-specific

299 CTLA4Ig, alpha-CD40L and alpha-CD25 accepted skin grafts without further immunosuppression.

300 (82% acceptance, n = 19) as well as to donor skin grafts without recipient immunosuppression (57% acc