ライフサイエンスコーパス: skin graft

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

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

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

4 uces a rapid destruction of the transplanted skin graft.

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

6 al blood mononuclear cells allogeneic to the skin graft.

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

8 aring a LG-15 minor H antigen (ag)-disparate skin graft.

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

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

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

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

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

14 nance was observed in primarily vascularized skin grafts.

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

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

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

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

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

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

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

22 s tested using mixed lymphocyte cultures and skin grafts.

23 allograft survival accepted ACI but not PVG skin grafts.

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

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

26 two of four animals rejecting delayed donor skin grafts.

27 tivated exocytosis and inflammation in human skin grafts.

28 olonged survival of minor antigen-mismatched skin grafts.

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

30 ly are able to effectively reject allogeneic skin grafts.

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

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

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

34 of fibroblasts and keratinocytes in cultured skin grafts.

35 tence of injected cells which share MHC with skin grafts.

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

37 tion accelerated rejection of syngeneic male skin grafts.

38 then received donor-specific and third-party skin grafts.

39 ), and donor-specific tolerance to secondary skin grafts.

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

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

42 nor acceleration of rejection of allogeneic skin grafts.

43 and cardiac transplants but not conventional skin grafts.

44 and prevent normal pigmentation of resulting skin grafts.

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

46 arget antigen and to rejection of autologous 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 sured by mixed lymphocyte reaction assay and skin grafting.

52 burn excision and autologous split-thickness skin grafting.

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

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

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

56 Injection of each cell type before skin grafting abolished hemopoietic cell engraftment and

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

58 2 deficiency and led to long-term allogeneic skin graft acceptance.

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

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

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

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

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

64 Swine donors were presensitized by mouse skin grafting and boosted by the injection of mouse cell

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

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

67 himeras without donor T cells rejected donor skin grafts and demonstrated strong antidonor reactivity

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

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

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

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

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

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

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

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

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

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

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

79 were collected at various times after mouse skin grafting, and their potential to induce GVHD and to

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

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

82 When C.B-17 SCID/beige mice bearing human skin grafts are injected i.p. with human PBMC allogeneic

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

103 /c grafts, but sensitized to third-party C3H skin grafts, demonstrated normally primed ex vivo IFN-ga

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

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

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

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

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

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

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

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

112 Skin grafting experiments between Snd/Snd and control mi

113 Skin grafting experiments confirmed the stratum corneum

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

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

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

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

118 e of chimeric animals retained donor-derived skin grafts for more than 120 days without requiring add

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

120 IMA was also found to extend the survival of skin grafts from a semiallogeneic donor (p < 0.02).

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

122 Skin grafts from animals with different AIB1 genotypes a

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

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

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

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

127 Skin grafts from mice expressing human bullous pemphigoi

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

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

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

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

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

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

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

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

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

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

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

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

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

141 In human skin grafts implanted on immunodeficient mice, administr

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

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

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

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

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

147 ies to achieve tolerance to fully mismatched skin grafts in euthymic mice.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

168 C developed an inflammatory reaction without skin graft loss.

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

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

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

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

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

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

175 morphology was investigated using 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 5(+) T cells were found within the tolerated skin grafts of long-term tolerant recipients.

184 2(b/d)) BMCs on day 7 relative to DBA/2 (D2) skin grafting on day 0.

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

186 Murine recipients of allogeneic skin grafts on day 0 were either untreated or given a DS

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

188 human T cells infiltrating allogeneic human skin grafts on human huPBL-SCID/bg mice, an in vivo mode

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

205 Skin graft recipients with exposures to animals may be a

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

228 ansplantation of Flt3L(-)/(-) heart, but not skin grafts, respectively.

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

230 Injection of presensitized cells after skin grafting resulted in different outcomes depending o

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

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

233 re combined immunodeficiency mice with human skin grafts (SCIDhu mice) indicate that VZV infection of

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

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

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

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

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

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

240 Skin graft survival and healing requires rapid restorati

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

242 Skin graft survival on high CD47 recipients was prolonge

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

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

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

246 Skin graft survival was unaffected.

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

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

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

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

251 TSP1 through CD47 limits skin graft survival.

252 autoimmune colitis, and prolongs allogeneic skin graft survival.

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

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

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

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

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

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

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

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

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

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

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

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 Skin grafting unveiled additional defects in GATA-3-null

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

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

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

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

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

277 ed by the injection of mouse cells after the skin graft was rejected.

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 ndicating that acceptance of EGFP-expressing skin grafts was the result of specific immune tolerance

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

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

284 Healed skin grafts were also noted.

285 In both combinations, skin grafts were also rejected.

286 When syngeneic skin grafts were exchanged between gender-matched wild-t

287 Skin grafts were placed distal to the popliteal fossa an

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

289 Allogeneic skin grafts were rejected by recipients treated with ant

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

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

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