ライフサイエンスコーパス: heart graft

1 hen assessing the alloantibody response to a heart graft.

2 or B-cell reactivity in parental to F1 mouse heart grafts.

3 dherence to endothelium and extravasation in heart grafts.

4 crophages on the morphology of lymphatics in heart grafts.

5 ired localization of alloreactive T cells to 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 , acutely rejected fully allogeneic skin and heart grafts.

10 e-induced by IFN-gamma, (Mig), in allogeneic heart grafts.

11 also triggered the rejection of the primary 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 a heart graft, a heart graft and a VTL, or a heart graft and a donor thymocyte infusion.

16 Animals received a heart graft, a heart graft and a VTL, or a heart graft and a donor thym

17 Heart grafts and blood samples, harvested on days 3, 5,

18 Tolerance was assessed by skin and heart grafts and enzyme-linked immunospot, intracellular

19 e long-term survival of MHC-mismatched mouse heart grafts and inhibition of alloantibody production.

20 than their counterparts that received only a heart graft, and those receiving 28 days of tacrolimus m

21 ing grafts, or by rejection of the challenge heart grafts, and by in vitro immune assay.

22 T cells to bone marrow grafts combined with heart grafts, and compared murine graft and host surviva

23 s induce tolerance to donor-matched neonatal heart grafts, and one way the HSC grafts alter host immu

24 but all rats are operationally tolerant; the heart grafts are accepted and remain beating for more th

25 LBNF1 heart grafts are rejected in an accelerated manner withi

26 ks of age; group 2 rats received only an ACI heart graft at 8 to 10 weeks.

27 roduces mild prolongation in survival of rat heart grafts, but has no significant effect on chronic g

28 in the rejection of complete MHC-mismatched heart grafts by CCR5(-/-) recipients were directly inves

29 d expression of CD1d on donor marrow but not heart graft cells.

30 In some hearts, graft cells formed adherens and gap junctions wi

31 ient (DAF KO; B6129F2 H-2) mice were used as heart graft donors to alpha1,3-galactosyltransferase def

32 Paradoxically, heart grafts elicited a stronger proliferation and effec

33 acute cellular rejection grading scheme for heart graft endomyocardial biopsy specimens (EMBs).

34 extended to fully allogeneic C57BL/6 skin or heart grafts, even in recipients that had accepted K ski

35 M alone or BM + FL resulted in uniform early heart graft failure (MST < 8 days).

36 e to induce tolerance to alphaGal-expressing heart grafts following a lethal dose of irradiation.

37 s accepted fully allogeneic DBA/2 (H-2(d/d)) heart grafts for >180 days, while similar transplants we

38 ipients not pretreated with CsA accepted LEW heart grafts for greater than 90 days.

39 and liver transplant (H+LTx) can protect the heart graft from the development of cardiac allograft va

40 Heart grafts from A/J (H-2(a)) donors were rejected by w

41 e receiving skin or vascularized heterotopic heart grafts from C57Bl/6 mice.

42 By contrast, heart grafts from CD4 T-cell-depleted donors developed o

43 The virus is consistently detected in the heart grafts from day 7 until day 35 posttransplantation

44 In contrast, long-surviving heart grafts from the Lewis orthotopic liver allograft p

45 Histological examination of long-term heart grafts (>100 days) demonstrated chronic rejection,

46 nd permanently accepted donor-type GalT(+/+) heart grafts (>150 days), whereas non-BMT control animal

47 g long-term survival of fully MHC-mismatched heart grafts, histologic analysis of long-surviving hear

48 +, B7-2bright), many of which rejected their heart grafts in an accelerated fashion.

49 The heart grafts in both groups undergo a transient acute re

50 ally transplanted A/J (H-2(a)) and syngeneic heart grafts in C57BL/6 (H-2(b)) recipient mice from 1.5

51 or-specific BALB/c, but not third party C3H, heart grafts in CD8-deficient C57BL/6 recipients.

52 to induce long-term acceptance of allogeneic heart grafts in mice, the induction of T(reg) cells was

53 sufficient to induce long-term tolerance to heart grafts in mice.

54 mma perfusion had no demonstrable effects on hearts grafts in tolerant recipients or on autologous he

55 injected with donor antigens accepted donor heart grafts indefinitely when compared with control rec

56 iciently inbred to accept first set skin and heart grafts indefinitely.

57 iving 28 days of tacrolimus maintained their heart grafts long-term.

58 cute and chronic rejection in a vascularized heart graft model and to compare this regimen with other

59 es resulted in acute rejection of B6.H-2bm12 heart grafts only if CD25+ cells were depleted.

60 When syngeneic heart grafts or liver nonparenchymal cells were transpla

61 e reconstituted with GalT accepted alphaGal+ heart grafts over 100 days.

62 The heart-graft-primed T cells transiently infiltrated the g

63 Bm12.Kd.IE heart grafts provoked strong germinal centre alloantibod

64 T cells within MHC class II-mismatched bm12 heart grafts provokes antinuclear humoral autoimmunity i

65 No donor-derived cells were propagated from heart graft recipients given either tacrolimus or donor

66 ctivity was persistently elevated in control heart graft recipients with comparatively low levels of

67 Four heart graft recipients with no evidence of chronic rejec

68 icrog/d, days 0-6) significantly accelerated heart graft rejection both in the B10-->C3H (mean surviv

69 , FcgammaRIIb-mediated inhibition of B6.K(d) heart graft rejection was abrogated by increasing T cell

70 K cells from a C57BL/6 recipient of a BALB/c heart graft resulted in the development of autoantibody,

71 with donor cells enjoyed markedly prolonged heart graft survival and initially preserved histologica

72 ays before transplant markedly prolonged B10 heart graft survival in C3H recipients.

73 AAsTreg) to permit long-term, donor-specific heart graft survival in immunocompetent hosts.

74 cells prevent costimulatory blockade-induced heart graft survival in mice, but whether and how preexi

75 rolimus alone significantly prolonged median heart graft survival time from 10 to 22 days (P<0.001).

76 ndings is the observed prolongation of mouse heart graft survival when HO-1 is expressed in vivo in b

77 low-dose RAPA promoted indefinite (>100 day) heart graft survival.

78 cell proliferation and prolonged subsequent heart graft survival.

79 es to alloantigens and prolongs vascularized heart graft survival.

80 The results demonstrate allogeneic heart grafts survive long-term in mCTLA4Ig-treated B6 an

81 ulation blockade, busulfan, and bone marrow, heart grafts survived indefinitely without detectable si

82 H2-DMalpha(-/)- donor heart grafts survived three times longer than wild-type

83 ymphocyte and macrophage inflammation of the heart graft that accumulated in the endocardium and arte

84 s a donor-specific infectious tolerance of a heart graft that can be adoptively transferred to subseq

85 ation of a minor antigen (HY) sex-mismatched heart graft, the lymphatic flow index was significantly

86 al or histology of DST/MR1-treated syngeneic heart grafts, the latter indicating that persistent auto

87 nd more than 2 years for non-life-supporting heart grafts to less than 1 month for life-supporting li

88 Hearts grafted to hosts after C6 reconstitution by bone

89 A-Tg heart grafts transplanted into WT mice with abundant ant

90 Allogeneic heart grafts transplanted to wild-type, but not IFN-gamm

91 ents receiving a fully MHC-mismatched BALB/c heart graft treated with CTLA4Ig + donor-specific transf

92 so was loss of passenger leukocytes from the heart graft, up-regulation of cytokine mRNA and major hi

93 Heterotopic heart grafting was performed with or without presensitiz

94 duced by anti-CD4 treatment, and third-party heart grafts were acutely rejected without affecting sur

95 ection, Lewis recipients of Brown Norway rat heart grafts were left untreated for the first 5 days af

96 However, skin as well as heart grafts were permanently accepted in the CD4 knocko

97 Second donor-matched heart grafts were permanently accepted, whereas third-pa

98 C57BL/Ka, Thy-1.1 neonatal heart grafts were placed in reconstituted animals either

99 Long-term surviving hamster heart grafts were rejected after transfer of hyperimmune

100 Donor-matched heart grafts were transplanted into long-term surviving

101 3 would prolong allograft survival, neonatal heart grafts were transplanted to allogeneic recipients

102 (H-2k) mice transplanted with BALB/c (H-2d) heart grafts were treated i.v. with a 7-day osmotic pump

103 ng-term survival of partially MHC-mismatched heart grafts when combined with short-term adjunctive im

104 were generated in 10 long-term recipients of heart grafts with progressive chronic rejection and comp

105 nged 100 days later with a Lewis heterotopic heart graft without immunosuppression.