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1 6-Fc ameliorated rejection response to mouse heart allograft.
2 a fully mismatched C57BL/6 (H2b) heterotopic heart allograft.
3 0 mice) were used as donor or recipient of a heart allograft.
4 ted en bloc and co-transplanted with a donor heart allograft.
5 ion in mice that have been induced to accept heart allografts.
6 pients without displaying adverse effects on heart allografts.
7 ts, they failed to trigger rejection of GRKO heart allografts.
8 siveness in murine recipients of heterotopic heart allografts.
9 able to induce hyperacute rejection of GAL+ heart allografts.
10 immunized GALT/KO mice as recipients of GAL+ heart allografts.
11 r bone marrow cells develop tolerance to ACI heart allografts.
12 nism for the chronic rejection of kidney and heart allografts.
13 D to evaluate the reproducibility of CGVD in heart allografts.
14 onocytes facilitates long-term acceptance of heart allografts.
15 dly prolonged the survival of neonatal mouse heart allografts.
16 order to prevent the rejection of kidney or heart allografts.
17 differential diagnosis of acute rejection of heart allografts.
18 acceptance of donor-type but not third-party heart allografts.
19 ar Furth (RT1u) recipients of Buffalo (RT1b) heart allografts.
20 nsferred to congenic B6 recipients of BALB/c heart allografts.
21 ype heart allografts but not for CX3CR1(-/-) heart allografts.
22 ells are able to acutely reject skin but not heart allografts.
23 re necessary for maintenance of tolerance to heart allografts.
24 ds to long-term survival of H-2 incompatible heart allografts.
25 protein induced accelerated rejection of BN heart allografts.
26 induce accelerated rejection or tolerance of heart allografts.
27 ODN significantly prolonged the survival of heart allografts.
28 opment of oxidative stress in reperfused rat-heart allografts.
30 urvival of third-party Brown Norway (RT1.An) heart allografts (14.3+/-2.5 days) compared with FTY720
31 then received wild-type or ICAM-1-deficient heart allografts 3 days later, the primed recipients rej
32 ion of rejecting mouse heterotopic abdominal heart allografts 5 days after transplantation is depress
33 o induce transplantation tolerance toward WF heart allografts: a portal vein injection of alpha(1h)l/
35 ll activation, enabled long-term survival of heart allografts across a complete mismatch of the MHC i
36 -dose immunosuppression enables tolerance of heart allografts across a full major histocompatibility
37 ts show that low dose CO inhalation protects heart allografts and can considerably prolong their surv
38 (-/-) (H-2(b)) mice received B10.BR (H-2(k)) heart allografts and repeated doses of IgG2a, IgG1 or F(
39 e or chronic rejection of kidney, liver, and heart allografts and with development of allograft fibro
40 ction enhances the development of TVS in rat heart allografts, and this process is initiated between
41 ymphocytes, we found that newly transplanted heart allografts are rejected acutely, while healed-in a
42 th donor-specific primary liver, kidney, and heart allografts are significantly lower than rejection
43 at TLOs develop within chronically rejecting heart allografts, are predominantly B cell in origin, an
44 I (RT1a) rats reject Wistar-Furth (WF; RT1u) heart allografts at a mean survival time of 8.9+/-1.0 da
45 nt recipients rejected MHC class II-mismatch heart allografts at a much faster rate and showed a high
46 -Ig induced long-term survival for wild-type heart allografts but not for CX3CR1(-/-) heart allograft
47 ACI recipients were rendered tolerant to WF heart allografts by a single injection via the portal ve
49 of single class II MHC-disparate B6.H-2bm12 heart allografts by C57BL/6 recipients is inhibited by t
50 sms preventing acute rejection of B6.H-2bm12 heart allografts by C57BL/6 recipients were investigated
51 e have successfully induced tolerance to rat heart allografts by recipient pretreatment with a single
52 donor-specific acceptance of rejection-prone heart allografts by recipients pretreated with immature
53 ronic allograft vasculopathy (CAV) in murine heart allografts can be elicited by adoptive transfer of
54 or ability to cause complement deposition in heart allografts compared with Abs induced by Th1 cells,
55 ted by day 10-14 posttransplant, while FVB/N heart allografts continued to function in C57BL/6, BCKO,
56 ression levels of several chemokine genes in heart allografts correlate with histologic rejection gra
57 splanted; however, long-term survival of ACI heart allografts could be induced when heart transplants
59 erse effect on the survival of the first LEW heart allografts, demonstrating the specificity of the t
60 ng regimen failed to induce tolerance to the heart allografts despite the development of mixed chimer
61 e exposed to NIMA accepted permanently K(b+) heart allografts despite the presence of normal levels o
63 sed expression of T-cell chemoattractants in heart allografts during later rejection when compared wi
66 Tolerant ACI recipients bearing primary WF heart allografts for more than 100 days accepted second
67 but not third-party Brown Norway (BN; RT1n), heart allografts from 5.9 +/- 0.5 days in controls to 4.
69 hearts contained fewer dendritic cells, and heart allografts from CX3CR1(-/-) donors survived signif
71 iming and function of T cells in response to heart allografts from MHC-mismatched wild-type vs ICAM-1
72 examined the gene expression profiles of rat heart allografts from recipients treated with or without
74 with allografts from STAT5a/b+/+ recipients, heart allografts from STAT5a/b-/- recipients had markedl
75 sed and computerized measurements performed, heart allografts from tolerant recipients showed signifi
78 grafts (H-2d) were accepted, and third-party heart allografts (H-2k) were rejected by tolerant PKCthe
79 of heart allografts showed that tolerant BN heart allografts had no evidence of acute or chronic rej
80 ) and PI3Kdelta (D910A/D910A) mice receiving heart allografts have suppression of alloreactive T effe
82 term graft survivors rejected third-party BN heart allografts in 14 days without an adverse effect on
83 a protein induced permanent acceptance of WF heart allografts in 16 of 26 ACI recipients (>100 days);
87 -69-RT1.Aa only prolonged the survival of WF heart allografts in ACI hosts (14.0+/-0.8 days; P<0.01).
88 nor blood cells facilitates tolerance to ACI heart allografts in Lewis rat hosts given posttransplant
91 antigen presenting cells in the rejection of heart allografts in mice and differences among B7KO and
95 nduced tolerance to Brown Norway (BN) (RT1n) heart allografts in PVG (RT1c) recipients more effective
96 al of RT1.Aa-disparate PVG.R8 (RT1.AaDuBuCu) heart allografts in PVG.1U (RT1u) hosts from 6.3 +/- 0.5
98 nvestigated whether the long survival of the heart allografts in the pretreated mice was associated w
100 s involves clonal deletion, and tolerance to heart allografts in this model also involves regulatory
101 hypothesis, we compared survival of skin and heart allografts in wild-type (IFN-gamma+/+) mice to tha
102 SRL produced dose-dependent prolongation of heart allografts: in untreated controls, 0.5 mg/kg SRL p
103 ecent transcriptome analysis of CMV-infected heart allografts indicates that the virus induces cytoki
105 hich cotransplantation of a donor kidney and heart allograft induces tolerance to both organs in mini
108 es and continued acceptance of FVB/N-matched heart allografts is independent of host CD8+ T cells and
109 like cell lines, and immunostaining in human heart allografts localized the AIF-1 gene product to a s
111 F rats to reject in rapid fashion either LEW heart allografts (mean survival time [MST] = 4.2+/-0.4 d
113 rotocol into the acute Wistar-Furth to Lewis heart allograft model resulted in a mean graft survival
116 ed into C57BL/6 mice that had accepted FVB/N heart allografts more than 60 days (heart acceptor mice)
118 . 5.6+/-0.5 days in controls; P<0.001) or WF heart allografts (MST=4.4+/-0.6 days vs. 6.0+/-0.0 days
119 ved either an isolated MHC class I disparate heart allograft (n=3) or combined class I disparate hear
120 recipients bearing either class I disparate heart allografts (n=5) or heart and kidney allografts (n
122 dence that chronic rejection of vascularized heart allografts occurs in the complete absence of antib
124 D-1 blockade led to accelerated rejection of heart allografts only in CD28(-/-) and CD8(-/-)CD28(-/-)
126 vascularized and functional donor thymus to heart allograft recipients at the time of transplantatio
127 st to kidney allograft recipients, long-term heart allograft recipients eventually developed humoral
129 the donor-specific Ab produced in CCR5(-/-) heart allograft recipients is sufficient to directly med
130 sttransplant antidonor HLA antibodies in 168 heart allograft recipients transplanted from October 200
132 ll help is not limited to the use of mATG in heart allograft recipients, and it is observed in nontra
138 r-specific kidney is cotransplanted with the heart allograft, recipients become tolerant to donor ant
139 lockade of CSE with propargylglycine delayed heart allograft rejection and abrogated type IV hypersen
140 re we analyzed the role of mouse IgV-CD80 in heart allograft rejection and search for equivalent spli
141 or-derived dendritic cells resulted in acute heart allograft rejection by 4C T cells, demonstrating t
142 investigate the role of macrophages in acute heart allograft rejection by cellular and functional MRI
143 ers of IgG alloantibodies that contribute to heart allograft rejection in CD40-/- heart recipients.
145 fective at constraining B cell responses and heart allograft rejection in sensitized recipients.
147 ther indirect allorecognition is involved in heart allograft rejection T cells obtained from peripher
148 rred to Rag1-/- recipients failed to mediate heart allograft rejection until supplemented with STAT5a
155 ivate more H-2K(b)-specific T cells in vivo; heart allografts stimulate the activation and proliferat
156 othelial venules) were detectable in 9 of 13 heart allografts studied and were predominantly B cell i
157 /6 recipients of fully MHC-mismatched BALB/c heart allografts, suggesting the possible generation of
158 T cell-specific pan-Notch blockade prolonged heart allograft survival and decreased IFN-gamma and IL-
160 ndirect pathway T-cell responses and prolong heart allograft survival but fail to directly regulate T
161 0.05-8.0 mg/kg/day) by oral gavage prolonged heart allograft survival in dose-dependent fashion.
162 mulation pathways induces long-term skin and heart allograft survival in IFN-gamma+/+ recipients but
164 d hematopoietic chimerism leads to long-term heart allograft survival in MHC disparate monkeys withou
166 mouse (m) IL-10 on heterotopic vascularized heart allograft survival in the B10(H2b)-->C3H(H2k) stra
170 he ME C-raf antisense oligos produced better heart allograft survival rates than did PS C-raf oligo.
171 l antidonor T cell responses, and prolonging heart allograft survival than the commonly used treatmen
172 D40, CD80, CD86)-deficient can prolong mouse heart allograft survival This is associated with microch
173 T1.Aa-Sf9 or ms/RT1.Aa-Sf9 cells reduced ACI heart allograft survival to 3.8 +/- 0.4 days or 3.7 +/-
174 -100) was remarkably effective in prolonging heart allograft survival to a median of >100 from 45 day
178 in rhesus monkeys would cause: (1) prolonged heart allograft survival, (2) inhibition of primary but
180 f oral SRL and CsA synergistically prolonged heart allograft survival, as documented by combination i
181 olimus (SRL) acted synergistically to extend heart allograft survival, the effect was potentiated by
182 ells at the time of transplant prolonged C3H heart allograft survival, whereas FL-BM cells did not.
183 ls, recombinant EPO administration prolonged heart allograft survival, whereas pharmacologic downregu
184 -mismatched (C3HHeJ; C3H(H-2k)) vascularized heart allograft survival, with long-term (>100 days) don
190 with heart allografts from WT mice, Tim4-/- heart allografts survived much longer and were more easi
191 nscriptional decrease in FOXO1 expression in heart allografts that is localized to both the cardiomyo
192 that CD8 T-cell-mediated rejection of murine heart allografts that lack hematopoietic APCs requires h
193 ntibodies and chronic rejection of kidney or heart allografts, the clinical significance of anti-HLA
194 f animals bearing isolated class I disparate heart allografts, the thymectomized recipients rejected
195 cells triggered acute rejection of wild-type heart allografts, they failed to trigger rejection of GR
196 destruction of passenger lymphocytes within heart allografts, this process occurs too slowly to prev
197 allograft injury, we tested the rejection of heart allografts transgenically expressing a single clas
199 of syngeneic grafts and ACI recipients of WF heart allografts treated with high-dose CsA (10 mg/kg/da
200 ewis (LEW) liver, bone marrow cell (BMC) and heart allografts under a brief course of tacrolimus.
201 Lewis rats were rendered tolerant to ACI heart allografts using a regimen of posttransplant total
203 sponses in the absence of CD28, rejection of heart allografts was studied in CD28-deficient mice.
204 fected COS7 cell cultures and in transfected heart allografts were examined by enzyme immunoassay (EI
207 cepted, whereas third-party (Sprague-Dawley) heart allografts were rejected by the tolerant recipient
213 urth (RT1u) rat recipients of Buffalo (RT1b) heart allografts were treated with FTY720 alone or in co
214 ients of heterotopic vascularized B10 (H-2b) heart allografts were treated with recombinant (r) mouse
216 nduce a similar survival of Brown Norway rat heart allografts with an equal suppression of intragraft
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