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1 hen assessing the alloantibody response to a heart graft.
2 , acutely rejected fully allogeneic skin and heart grafts.
3 or B-cell reactivity in parental to F1 mouse heart grafts.
4 dherence to endothelium and extravasation in heart grafts.
5 crophages on the morphology of lymphatics in heart grafts.
6 priming and in acute rejection of B6.H-2bm12 heart grafts.
7 gan donors or recipients of MHC-incompatible heart grafts.
8 ian survival of fully allogeneic heterotopic heart grafts.
9 e-induced by IFN-gamma, (Mig), in allogeneic heart grafts.
10  also triggered the rejection of the primary heart grafts.
11 ired localization of alloreactive T cells to heart grafts.
12 e for encoding rat xenoantibodies to hamster heart grafts.
13 t promptly rejected third-party Brown Norway heart grafts (9.3+/-1.5 days).
14                           Animals received a heart graft, a heart graft and a VTL, or a heart graft a
15 ocompatibility-antigen mismatched allogeneic heart grafts, a robust immune response was mounted to ea
16 vement of antibody-mediated rejection and to heart graft access.
17 a heart graft, a heart graft and a VTL, or a heart graft and a donor thymocyte infusion.
18            Animals received a heart graft, a heart graft and a VTL, or a heart graft and a donor thym
19                                              Heart grafts and blood samples, harvested on days 3, 5,
20           Tolerance was assessed by skin and heart grafts and enzyme-linked immunospot, intracellular
21 e long-term survival of MHC-mismatched mouse heart grafts and inhibition of alloantibody production.
22 o examine CD45(+) immune cells from both the heart grafts and spleens.
23 than their counterparts that received only a heart graft, and those receiving 28 days of tacrolimus m
24 ing grafts, or by rejection of the challenge heart grafts, and by in vitro immune assay.
25  T cells to bone marrow grafts combined with heart grafts, and compared murine graft and host surviva
26 s induce tolerance to donor-matched neonatal heart grafts, and one way the HSC grafts alter host immu
27 but all rats are operationally tolerant; the heart grafts are accepted and remain beating for more th
28                                        LBNF1 heart grafts are rejected in an accelerated manner withi
29 s serious adverse events associated with the heart graft at 30 days after transplantation.
30 f serious adverse events associated with the heart graft at 30 days after transplantation.
31 ks of age; group 2 rats received only an ACI heart graft at 8 to 10 weeks.
32 roduces mild prolongation in survival of rat heart grafts, but has no significant effect on chronic g
33  in the rejection of complete MHC-mismatched heart grafts by CCR5(-/-) recipients were directly inves
34 d expression of CD1d on donor marrow but not heart graft cells.
35                                      In some hearts, graft cells formed adherens and gap junctions wi
36 ient (DAF KO; B6129F2 H-2) mice were used as heart graft donors to alpha1,3-galactosyltransferase def
37                               Paradoxically, heart grafts elicited a stronger proliferation and effec
38  acute cellular rejection grading scheme for heart graft endomyocardial biopsy specimens (EMBs).
39 extended to fully allogeneic C57BL/6 skin or heart grafts, even in recipients that had accepted K ski
40 M alone or BM + FL resulted in uniform early heart graft failure (MST < 8 days).
41 e to induce tolerance to alphaGal-expressing heart grafts following a lethal dose of irradiation.
42 s accepted fully allogeneic DBA/2 (H-2(d/d)) heart grafts for >180 days, while similar transplants we
43 ipients not pretreated with CsA accepted LEW heart grafts for greater than 90 days.
44 and liver transplant (H+LTx) can protect the heart graft from the development of cardiac allograft va
45                                              Heart grafts from A/J (H-2(a)) donors were rejected by w
46 e receiving skin or vascularized heterotopic heart grafts from C57Bl/6 mice.
47                                 By contrast, heart grafts from CD4 T-cell-depleted donors developed o
48    The virus is consistently detected in the heart grafts from day 7 until day 35 posttransplantation
49                  In contrast, long-surviving heart grafts from the Lewis orthotopic liver allograft p
50 nsin solution (n = 7) significantly protects heart graft function, measured by quantitative ultrasoun
51        Histological examination of long-term heart grafts (&gt;100 days) demonstrated chronic rejection,
52 nd permanently accepted donor-type GalT(+/+) heart grafts (&gt;150 days), whereas non-BMT control animal
53 g long-term survival of fully MHC-mismatched heart grafts, histologic analysis of long-surviving hear
54 +, B7-2bright), many of which rejected their heart grafts in an accelerated fashion.
55                                          The heart grafts in both groups undergo a transient acute re
56 ally transplanted A/J (H-2(a)) and syngeneic heart grafts in C57BL/6 (H-2(b)) recipient mice from 1.5
57 or-specific BALB/c, but not third party C3H, heart grafts in CD8-deficient C57BL/6 recipients.
58 to induce long-term acceptance of allogeneic heart grafts in mice, the induction of T(reg) cells was
59  sufficient to induce long-term tolerance to heart grafts in mice.
60 IgE was found on acute rejection of skin and heart grafts in several murine strain combinations, as w
61 mma perfusion had no demonstrable effects on hearts grafts in tolerant recipients or on autologous he
62  injected with donor antigens accepted donor heart grafts indefinitely when compared with control rec
63 iciently inbred to accept first set skin and heart grafts indefinitely.
64 iving 28 days of tacrolimus maintained their heart grafts long-term.
65 cute and chronic rejection in a vascularized heart graft model and to compare this regimen with other
66 es resulted in acute rejection of B6.H-2bm12 heart grafts only if CD25+ cells were depleted.
67                               When syngeneic heart grafts or liver nonparenchymal cells were transpla
68 e reconstituted with GalT accepted alphaGal+ heart grafts over 100 days.
69                                          The heart-graft-primed T cells transiently infiltrated the g
70                                   Bm12.Kd.IE heart grafts provoked strong germinal centre alloantibod
71  T cells within MHC class II-mismatched bm12 heart grafts provokes antinuclear humoral autoimmunity i
72 fficacy of infused darTreg in lymphodepleted heart graft recipients appears to reflect loss of a regu
73  No donor-derived cells were propagated from heart graft recipients given either tacrolimus or donor
74 ctivity was persistently elevated in control heart graft recipients with comparatively low levels of
75                                         Four heart graft recipients with no evidence of chronic rejec
76 icrog/d, days 0-6) significantly accelerated heart graft rejection both in the B10-->C3H (mean surviv
77  rates were low, 4% (95% CI, 0%-22%), and no heart graft rejection greater than mild was reported.
78 , FcgammaRIIb-mediated inhibition of B6.K(d) heart graft rejection was abrogated by increasing T cell
79 -specific antibody responses and accelerated heart graft rejection.
80  as well as during chronic antibody-mediated heart graft rejection.
81 K cells from a C57BL/6 recipient of a BALB/c heart graft resulted in the development of autoantibody,
82  with donor cells enjoyed markedly prolonged heart graft survival and initially preserved histologica
83 ays before transplant markedly prolonged B10 heart graft survival in C3H recipients.
84 AAsTreg) to permit long-term, donor-specific heart graft survival in immunocompetent hosts.
85 cells prevent costimulatory blockade-induced heart graft survival in mice, but whether and how preexi
86 rolimus alone significantly prolonged median heart graft survival time from 10 to 22 days (P<0.001).
87 ndings is the observed prolongation of mouse heart graft survival when HO-1 is expressed in vivo in b
88 unoregulatory pathway that prolongs skin and heart graft survival.
89 low-dose RAPA promoted indefinite (>100 day) heart graft survival.
90  cell proliferation and prolonged subsequent heart graft survival.
91 es to alloantigens and prolongs vascularized heart graft survival.
92 ary outcome was transplantation of the donor heart; graft survival at 30 days after transplantation w
93           The results demonstrate allogeneic heart grafts survive long-term in mCTLA4Ig-treated B6 an
94 ulation blockade, busulfan, and bone marrow, heart grafts survived indefinitely without detectable si
95                        H2-DMalpha(-/)- donor heart grafts survived three times longer than wild-type
96 ymphocyte and macrophage inflammation of the heart graft that accumulated in the endocardium and arte
97 s a donor-specific infectious tolerance of a heart graft that can be adoptively transferred to subseq
98 ation of a minor antigen (HY) sex-mismatched heart graft, the lymphatic flow index was significantly
99 al or histology of DST/MR1-treated syngeneic heart grafts, the latter indicating that persistent auto
100 nd more than 2 years for non-life-supporting heart grafts to less than 1 month for life-supporting li
101                                              Hearts grafted to hosts after C6 reconstitution by bone
102                                         A-Tg heart grafts transplanted into WT mice with abundant ant
103                                   Allogeneic heart grafts transplanted to wild-type, but not IFN-gamm
104 ents receiving a fully MHC-mismatched BALB/c heart graft treated with CTLA4Ig + donor-specific transf
105 so was loss of passenger leukocytes from the heart graft, up-regulation of cytokine mRNA and major hi
106                                  Heterotopic heart grafting was performed with or without presensitiz
107 duced by anti-CD4 treatment, and third-party heart grafts were acutely rejected without affecting sur
108 ection, Lewis recipients of Brown Norway rat heart grafts were left untreated for the first 5 days af
109                     However, skin as well as heart grafts were permanently accepted in the CD4 knocko
110                         Second donor-matched heart grafts were permanently accepted, whereas third-pa
111                   C57BL/Ka, Thy-1.1 neonatal heart grafts were placed in reconstituted animals either
112                  Long-term surviving hamster heart grafts were rejected after transfer of hyperimmune
113                                Donor-matched heart grafts were transplanted into long-term surviving
114 3 would prolong allograft survival, neonatal heart grafts were transplanted to allogeneic recipients
115  (H-2k) mice transplanted with BALB/c (H-2d) heart grafts were treated i.v. with a 7-day osmotic pump
116 ng-term survival of partially MHC-mismatched heart grafts when combined with short-term adjunctive im
117 were generated in 10 long-term recipients of heart grafts with progressive chronic rejection and comp
118 nged 100 days later with a Lewis heterotopic heart graft without immunosuppression.

 
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