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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.
36 of these mice challenged with donor-matched skin allografts accept these skin grafts, demonstrating
38 operative LM infection prevented cardiac and skin allograft acceptance induced by anti-CD154 and dono
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
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
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
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
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
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
75 e C57BL/6 allograft donors, and B6.H-2(bm12) skin allografts had a 5-day prolonged survival in B6.Mig
78 of human Tregs to prevent the rejection of a skin allograft in vivo, highlighting the therapeutic pot
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
85 reatment significantly prolonged survival of skin allografts in naive recipients as well as heart all
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
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
104 histocompatibility complex-mismatched murine skin allograft model to study graft survival and mechani
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
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
119 ells have been shown to be involved in acute skin allograft rejection in an ectothermic vertebrate.
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
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
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
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
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
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
171 154 mAb plus DST treatment failed to prolong skin allograft survival in nondiabetic male NOD mice.
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
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
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
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.
217 of alloreactive T cells and produced stable skin allograft tolerance, a very stringent test of allog
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
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
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
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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