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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  were adoptively transferred to mice-bearing skin allograft.
5 CD8-deficient mice can vigorously reject the skin allografts.
6 ransplantation tolerance to fully mismatched skin allografts.
7 oietic chimerism but it led to rapid loss of skin allografts.
8 ion response of naive T cells to established skin allografts.
9 ed immune privilege and survived longer than skin allografts.
10 us rejection and were eliminated faster than skin allografts.
11 lege and have good survival as compared with skin allografts.
12 rneal tissue than when they are expressed in skin allografts.
13 ion of full-thickness, MHC-mismatched rhesus skin allografts.
14 r non-donor neonatal porcine or mouse BALB/c skin allografts.
15 nd accepted donor-origin but not third-party skin allografts.
16 n BALB/c (H-2d) recipients of C57BL/6 (H-2b) skin allografts.
17 e tolerance to the more resistant kidney and skin allografts.
18 eral lymph nodes and subsequently migrate to skin allografts.
19 nocytes mediate the angiogenesis response in skin allografts.
20 nt engraftment of cardiac allografts but not skin allografts.
21 iated with the cell infiltrates in the human skin allografts.
22 Foxp3(+) T cells protect full MHC-mismatched skin allografts.
23 elf' and capable of rejecting MHC-mismatched skin allografts.
24 onged and even indefinite survival of OVA(+) skin allografts.
25 ism, and shortens survival of donor-specific skin allografts.
26 tiation factor 88 promotes the acceptance of skin allografts.
27 readily reject allogeneic cells, but not the skin allografts.
28 ation in muscles that received MT but not in skin allografts.
29 occurs at the onset of tissue destruction of skin allografts.
30 poresponsive CD4 T cells also fail to reject skin allografts.
31  nodes and are able to infiltrate and reject skin allografts.
32  HSCs and induce donor-specific tolerance to skin allografts.
33 s to reject same donor, but not third-party, skin allografts.
34 er of tolerance to heart and kidney, but not skin, allografts.
35                        After implantation of skin allografts, AAT-treated mice had greater numbers of
36  of these mice challenged with donor-matched skin allografts accept these skin grafts, demonstrating
37 pressive regimen, reliably induces permanent skin allograft acceptance in this model.
38 operative LM infection prevented cardiac and skin allograft acceptance induced by anti-CD154 and dono
39                             (c) Induction of skin allograft acceptance initially depended on the pres
40 on of DST uniformly results in long-term Ld+ skin-allograft acceptance.
41                    In RAG(-/-) recipients of skin allografts adoptively transferred with CD4(+) T cel
42    LPL(-/-) mice showed delayed rejection of skin allografts after release from immunosuppression.
43                                  Remarkably, skin allografts also were rejected acutely by splenectom
44       By using an adoptive transfer model of skin allograft and using specific Vbeta TCR probes, we d
45 ates with delayed rejection of MHC-disparate skin allografts and an impaired immune response against
46    We orthotopically transplanted mouse tail skin allografts and estimated the numbers of transcripts
47  mice are permissive for the growth of human skin allografts and human peripheral blood mononuclear c
48  cells we sought their presence in tolerated skin allografts and in normal skin.
49 ionally suppressive but failed to migrate to skin allografts and inhibit rejection.
50 ance of primary and secondary donor-specific skin allografts and rejection of third-party grafts.
51 demonstrated the vigorous rejection of human skin allografts and the absence of injury to porcine ski
52  abrogate B6.muMT(-/-) mice rejection of A/J skin allografts and this rejection rendered these recipi
53 r histocompatibility complex (MHC) disparate skin allografts and to test cellular and molecular chang
54 d in the frog Xenopus by antibody depletion, skin allografting, and tumor transplantation.
55 s for the difference in survival of islet vs skin allografts are not known.
56 g led to enhanced survival of heart, but not skin, allografts associated with impaired localization o
57 he kidney capsule of NNR allografts, but not skin allografts, at 12 days and beyond implies that NNR
58  The tolerant mice accepted the second donor skin allografts but acutely rejected the third-party gra
59 med mice eliminated accelerated rejection of skin allografts but failed to induce tolerance.
60 nged survival of kidney, islet, cardiac, and skin allografts, but again most animals have eventually
61 treatment could not block acute rejection of skin allografts, but interfered with sensitization for s
62 diabetes, nonetheless resist prolongation of skin allografts by costimulation blockade.
63 e showed in a skin transplant model that the skin allografts contain a subset of antigen-presenting c
64     B6AF1 mice received ALS (days -1 and 2), skin allografts (day 0), and BMC and/or thymus grafts (T
65 long-term survival of highly antigenic donor skin allografts despite the presence of functionally int
66 d deletion in the Mig gene were used as both skin allograft donors and recipients in a class II major
67 pressed by CTLs that infiltrate HY-disparate skin allografts during rejection.
68 ex in recipient livers promotes tolerance to skin allografts, even in animals primed to produce a mem
69 length of TCRs expressed by CTL-infiltrating skin allografts expressing the immunogenic H4 peptide du
70 d IFN-gamma), whereas primarily vascularized skin allografts failed to trigger a significant indirect
71 l effectors of microvascular injury in human skin allografts following adoptive transfer into immunod
72 al, and 40% of the recipients accepted their skin allograft for >100 days.
73               Moreover, when we transplanted skin allografts from stable tolerant chimeras onto synge
74 s, even in animals that had already rejected skin allografts from the same donors.
75 e C57BL/6 allograft donors, and B6.H-2(bm12) skin allografts had a 5-day prolonged survival in B6.Mig
76                            The acceptance of skin allografts has historically been among the most cha
77                                              Skin allograft in mice was used as an experimental trans
78 of human Tregs to prevent the rejection of a skin allograft in vivo, highlighting the therapeutic pot
79 regs to regulate immune responses to a human skin allograft in vivo.
80 cells (BMC) effectively induces tolerance to skin allografts in antilymphocyte serum- and rapamycin-t
81 ministration of LPS shortens the survival of skin allografts in mice treated with costimulation block
82 ock tolerance induction to hematopoietic and skin allografts in mice treated with costimulation block
83 reactive T cells, and indefinite survival of skin allografts in mice.
84  induces robust transplantation tolerance to skin allografts in mice.
85 reatment significantly prolonged survival of skin allografts in naive recipients as well as heart all
86 e capacity to induce rejection of HA bearing skin allografts in syngeneic hosts.
87 phocytes up-regulate Foxp3 in mice receiving skin allografts in the absence of any treatment.
88 ls led to significantly delayed rejection of skin allografts in the Balb/C->C57BL/6J model.
89 o intratesticular islet allografts spread to skin allografts in the non-privileged sites.
90 In contrast, nonimmunosuppressed cardiac and skin allografts in the same strain combination are rejec
91 nal in the trafficking of human T cells into skin allografts in vivo in the humanized SCID mouse.
92 CD200 mice with long-term surviving cardiac (skin) allografts in the absence of continued transgene i
93  wild-type mice and accelerated rejection of skin allografts, indicating that regulation of homeostat
94 show that long-term survival of vascularized skin allografts induced by anti-CD40L Abs was associated
95 , or OX40 ligand in this model reduces human skin allograft injury and T cell effector molecule expre
96                                      A human skin allograft injury model in immunodeficient mice, eng
97 demonstrate that the survival of human fetal skin allografts is markedly prolonged compared with that
98 gorously rejected fully MHC-mismatched DBA/2 skin allografts (mean survival time, 12 days; n = 6) com
99  molecules critical to T cell rolling within skin allograft microvasculature during the effector phas
100 onkeys were transplanted with full-thickness skin allografts mismatched at both class I and class II
101                         Here we used a mouse skin allograft model and an allogeneic radiation chimera
102                                      Using a skin allograft model in which transplant acceptance is c
103  several points has been examined in a mouse skin allograft model of this protocol.
104 histocompatibility complex-mismatched murine skin allograft model to study graft survival and mechani
105          To explore this role, we employed a skin allograft model using mice with targeted deletion o
106                            Unlike the murine skin allograft model, all grafts were rejected within 11
107            Using a highly immunogenic murine skin allograft model, we found that the absence of both
108 n immune responsiveness was examined using a skin allograft model.
109 vo CD44(+)CD8(+) T cells rejected donor-type skin allografts more rapidly than naive CD8(+) T cells d
110 rolonged survival of fully mismatched BALB/c skin allografts on C57BL/6 recipients, with approximatel
111  directs T cell infiltration into B6.H-2bm12 skin allografts on C57BL/6 recipients.
112  uniformly achieves >90-d survival of BALB/c skin allografts on C57BL/6 recipients.
113 onatal donors prolongs the survival of adult skin allografts on rabbit anti-mouse lymphocyte serum-tr
114 required to achieve prolonged engraftment of skin allograft or tolerance to islet allograft in recipi
115 ter characterize alloreactivity in naive and skin allograft-primed mice, we used a modified, high-res
116 requirement for regulatory CD4(+) T cells in skin allograft recipients could account for this differe
117    By contrast, B cell depletion exacerbated skin allograft rejection and augmented the proliferation
118                             The mechanism of skin allograft rejection has been thought to require pre
119 ells have been shown to be involved in acute skin allograft rejection in an ectothermic vertebrate.
120  the efficacy of hu5C8 in preventing primary skin allograft rejection in rhesus monkeys.
121 d are surprisingly potent in mediating acute skin allograft rejection in the absence of any adaptive
122 X40 costimulation is critically important in skin allograft rejection in this model, as blocking the
123                                              Skin allograft rejection in this system occurred in the
124 ules in vitro and can reduce T cell-mediated skin allograft rejection in vivo.
125      Similarly, in vivo, anti-OX40 prevented skin allograft rejection mediated by CD8+ T cells.
126 blockade of OX40-OX40L interactions prevents skin allograft rejection mediated by either subset of T
127 feration or donor Ag priming, induced prompt skin allograft rejection regardless of CD28/CD154 blocka
128 dy, we used a CD8(+) TCR transgenic model of skin allograft rejection to characterize in vivo activit
129 istant CD4(+)OX40(+) cells failed to mediate skin allograft rejection upon adoptive transferring into
130  KA1010 displayed no significant features of skin allograft rejection upon histological analysis at 7
131 able to abolish the stable MC nor to trigger skin allograft rejection, a hallmark of peripheral, not
132 dy, hu5C8, greatly delays the onset of acute skin allograft rejection.
133 ays does not adequately inhibit CD8-mediated skin allograft rejection.
134 CTL-detected peptides primed for accelerated skin allograft rejection.
135 d in a murine model for CD4+ T cell-mediated skin allograft rejection.
136 gs from the OX40(+) cells resulted in prompt skin allograft rejection.
137  vivo cytotoxicity assay and correlated with skin allograft rejection.
138 8/CD154 blockade had no effect in preventing skin allograft rejection.
139 of CD4+ T cells to reject class I mismatched skin allografts remains controversial.
140 let allograft tolerance induction; 2) unlike skin allografts, resistance to islet allograft tolerance
141     Re-exposure of C57BL/6 mice to HLA.A2(+) skin allografts resulted in a surge of donor-specific (a
142 n by Treg that simultaneously infiltrate the skin allografts, resulting in a failure to generate dono
143 ty in mice that rejected fully MHC-disparate skin allografts revealed a high frequency of interferon
144 vitro data, analysis of lymph nodes draining skin allografts revealed that OX40 blockade had no effec
145 NZW H2(z); or BALB/c H2(d)) heart, aorta, or skin allograft significantly compared with treatment wit
146 act hypersensitivity responses and tolerated skin allografts significantly longer than wild-type mice
147  allografts were unable to reject B6.H-2bm12 skin allografts, suggesting potential down-regulatory me
148 n with CD28/CD154 blockade induced long term skin allograft survival (>100 days; n = 5).
149   SC4 was also able to significantly prolong skin allograft survival across a MHC class I barrier.
150 arrow-cell (BMC) infusion induces indefinite skin allograft survival across fully mismatched mouse st
151                                          (3) Skin allograft survival after adoptive transfer of MDSCs
152 dents demonstrated prolongation of heart and skin allograft survival after peptide therapy.
153 yte serum (ALS) and sirolimus (Sir) prolongs skin allograft survival and produces chimerism.
154             Previous studies have shown that skin allograft survival can be augmented by the administ
155 ection sensitive to rapamycin, and long term skin allograft survival can be readily induced by rapamy
156      Costimulation blockade fails to prolong skin allograft survival in (NOD x C57BL/6)F1 mice and in
157 n of sirolimus (rapamycin) to induce maximal skin allograft survival in ALS-treated, BM-infused recip
158 atment with DST and anti-CD154 mAb prolonged skin allograft survival in both C57BL/6 (H2b) and C57BL/
159  costimulatory pathways effectively promotes skin allograft survival in C3H/HeJ mice, extending media
160 BL, or CD27/CD70 pathway, markedly prolonged skin allograft survival in CD28/CD154 DKO mice.
161 ive growth factor signals produced long term skin allograft survival in CD4-deficient mice (mean surv
162 locking OX40 costimulation induced long term skin allograft survival in CD4-deficient mice and CD8-de
163 affinity IL-2R, CD25, and IL-2 in prolonging skin allograft survival in mice receiving combined CD40/
164 c transfusion (DST) of spleen cells prolongs skin allograft survival in mice through a mechanism invo
165  are more potent than whole BM at prolonging skin allograft survival in mice treated with ALS and Sir
166 on of transplantation tolerance and shortens skin allograft survival in mice treated with costimulati
167  (mAb) induces permanent islet and prolonged skin allograft survival in mice.
168 ibody leads to permanent islet and prolonged skin allograft survival in mice.
169 thways has been shown to effectively promote skin allograft survival in mice.
170 herapy resulted in prolongation of heart and skin allograft survival in mice.
171 154 mAb plus DST treatment failed to prolong skin allograft survival in nondiabetic male NOD mice.
172 as been reported to induce long-term primary skin allograft survival in primates.
173  cells, or buffy coat cells led to prolonged skin allograft survival in recipients treated with anti-
174  node cells, or buffy coat cells can prolong skin allograft survival in recipients treated with costi
175 pon adoptive transfer, significantly prolong skin allograft survival in vivo.
176  treatment, and under such conditions stable skin allograft survival is difficult to achieve.
177                                 Induction of skin allograft survival requires the presence of CD4 cel
178 de enjoy a significantly greater increase in skin allograft survival than do wild-type mice.
179             Costimulation blockade prolonged skin allograft survival that was shortened after coinjec
180                                              Skin allograft survival was also prolonged in normal rec
181                                              Skin allograft survival was correlated with the recipien
182                                              Skin allograft survival was monitored, and the prolifera
183                                              Skin allograft survival was prolonged for up to 17.8+/-0
184 L/6 congenic mice with NOD-derived Idd loci, skin allograft survival was readily prolonged by costimu
185 ation blockade plus LPS also exhibited short skin allograft survival whereas similarly treated B6.CD8
186  CD4CD25 cells are required for induction of skin allograft survival, (2) CD4CD25 T cells are not req
187            We examined long-term cardiac and skin allograft survival, alloantigen-induced T-cell prol
188 n with CD28/CD154 blockade induced long-term skin allograft survival, and 40% of the recipients accep
189 X40 ligand pathway alone did not prolong the skin allograft survival, but blocking OX40 costimulation
190 al antibody (mAb) markedly prolongs heart or skin allograft survival, but the influence of this strat
191 5 cell deletion had no effect upon healed-in skin allograft survival.
192 deplete, peripheral chimerism and maintained skin allograft survival.
193 CD8(+) T cells and was associated with brief skin allograft survival.
194 es, costimulation blockade failed to prolong skin allograft survival.
195 s necessary but not sufficient for long-term skin allograft survival.
196            IDEC-131 modestly prolongs rhesus skin allograft survival.
197  and the gamma(c) pathways induced prolonged skin allograft survival.
198 ALS induces prolonged cardiac and second-set skin allograft survival.
199 row or donor splenocytes results in extended skin allograft survival.
200 allografts and dramatically prolongs primary skin allograft survival.
201  induce a significant prolongation in BALB/c skin allograft survival.
202 costimulatory molecules, and prolongation of skin allograft survival.
203 e of donor but not recipient MCP-1 prolonged skin allograft survival.
204 n of alloreactive CD8+ T cells and shortened skin allograft survival.
205 mediated T cell depletion markedly prolonged skin allograft survival.
206                                           BN skin allografts survived significantly longer on protein
207                                            A skin allograft system was used to demonstrate that disse
208 mmune responses to microbial antigens and to skin allografts, the prevailing view has been that the i
209 ombined immunodeficiency recipients of B10.A skin allografts, this cell line specifically induced a f
210 tion of thymectomy to the protocol permitted skin allografts to survive for > 100 d, suggesting that
211 a donor-specific transfusion or DST) permits skin allografts to survive for >100 days in thymectomize
212 etic basis for the resistance of NOD mice to skin allograft tolerance also applies to islet allograft
213 e hematopoietic chimerism and donor-specific skin allograft tolerance and justify further development
214 s study, we demonstrate that a stable MC and skin allograft tolerance can be established across MHC b
215  engraftment and induction of donor-specific skin allograft tolerance has recently been described.
216 ogeneic bone marrow engraftment and specific skin allograft tolerance induction.
217  of alloreactive T cells and produced stable skin allograft tolerance, a very stringent test of allog
218                                 In models of skin allograft tolerance, tumor growth, and experimental
219 ment increased durable donor-specific BALB/c skin allograft tolerance.
220 has been studied in several models including skin allograft tolerance.
221                   We studied the survival of skin allografts transplanted from fully allogeneic (BALB
222 stocompatibility complex disparate heart and skin allografts transplanted into CD8 knockout recipient
223 allowed permanent survival of heart, but not skin, allografts transplanted across a major histocompat
224 1l) to Buffalo (RT1b) rat cardiac, renal, or skin allograft was studied.
225          Tolerance to fully MHC-incompatible skin allografts was induced as follows: C57Bl/10 (H2b) r
226                       Modest prolongation of skin allografts was observed in mice reconstituted with
227 the associated angiogenesis reactions in the skin allografts were analyzed temporally by videomicrosc
228 unity, mice given costimulation blockade and skin allografts were coinjected with TLR2 (Pam3Cys), TLR
229 wever, after cessation of anti-OX40 therapy, skin allografts were eventually rejected indicating that
230 rafts survived long term (>84 days), whereas skin allografts were rapidly rejected ( approximately 13
231                                       BALB/c skin allografts were transplanted onto C57BL/6 Rag 1-/-
232                 C57BL/6 recipients of BALB/c skin allografts were treated with DSBM (150 x 10(6) cell
233                               Full-thickness skin allografts were used in C3H to B6AF1 (class I misma
234 ces specific unresponsiveness (tolerance) to skin allografts, which can be augmented by the adjuvant
235  proliferative response in vivo to heart and skin allografts, which in both cases was localized to re
236 ion, in contrast to that seen in response to skin allografts, which was delayed until 10-12 days afte
237 ating gene(-/-) mice, which received an H2b+ skin allograft with and without anti-OX40.
238 guingly, sorafenib prolonged the survival of skin allograft without major toxicity.
239 r-specific BM induced tolerance to renal and skin allografts without inducing hematopoietic chimerism
240 nontolerant lymphocytes from rejecting fresh skin allografts, without hindrance of rejection of third

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