ライフサイエンスコーパス: heart allograft

1 ted en bloc and co-transplanted with a donor heart allograft.

2 6-Fc ameliorated rejection response to mouse heart allograft.

3 a fully mismatched C57BL/6 (H2b) heterotopic heart allograft.

4 tolerance in recipients of a cotransplanted heart allograft.

5 besity, diabetes, malignancy, or a kidney or heart allograft.

6 0 mice) were used as donor or recipient of a heart allograft.

7 hibits antibody-mediated immune rejection of heart allografts.

8 opment of oxidative stress in reperfused rat-heart allografts.

9 ion in mice that have been induced to accept heart allografts.

10 ts, they failed to trigger rejection of GRKO heart allografts.

11 siveness in murine recipients of heterotopic heart allografts.

12 able to induce hyperacute rejection of GAL+ heart allografts.

13 immunized GALT/KO mice as recipients of GAL+ heart allografts.

14 r bone marrow cells develop tolerance to ACI heart allografts.

15 nism for the chronic rejection of kidney and heart allografts.

16 D to evaluate the reproducibility of CGVD in heart allografts.

17 onocytes facilitates long-term acceptance of heart allografts.

18 dly prolonged the survival of neonatal mouse heart allografts.

19 order to prevent the rejection of kidney or heart allografts.

20 differential diagnosis of acute rejection of heart allografts.

21 acceptance of donor-type but not third-party heart allografts.

22 ar Furth (RT1u) recipients of Buffalo (RT1b) heart allografts.

23 in C57BL/6 (B6) mice receiving A2-expressing heart allografts.

24 pients without displaying adverse effects on heart allografts.

25 of alloimmune responses and the rejection of heart allografts.

26 major histocompatibility complex-mismatched heart allografts.

27 nsferred to congenic B6 recipients of BALB/c heart allografts.

28 ype heart allografts but not for CX3CR1(-/-) heart allografts.

29 hatics and were recruited into donor-matched heart allografts.

30 ells are able to acutely reject skin but not heart allografts.

31 re necessary for maintenance of tolerance to heart allografts.

32 ds to long-term survival of H-2 incompatible heart allografts.

33 protein induced accelerated rejection of BN heart allografts.

34 induce accelerated rejection or tolerance of heart allografts.

35 ODN significantly prolonged the survival of heart allografts.

36 protein had no effect on the survival of WF heart allografts (10.5+/-0.6 days) in ACI hosts.

37 urvival of third-party Brown Norway (RT1.An) heart allografts (14.3+/-2.5 days) compared with FTY720

38 then received wild-type or ICAM-1-deficient heart allografts 3 days later, the primed recipients rej

39 ion of rejecting mouse heterotopic abdominal heart allografts 5 days after transplantation is depress

40 o induce transplantation tolerance toward WF heart allografts: a portal vein injection of alpha(1h)l/

41 D154, CD2, and CD28 is sufficient to prolong heart allograft acceptance or promote the expansion of r

42 interfere with the of mechanisms that permit heart allograft acceptance.

43 ll activation, enabled long-term survival of heart allografts across a complete mismatch of the MHC i

44 -dose immunosuppression enables tolerance of heart allografts across a full major histocompatibility

45 Cynomolgus monkeys were transplanted with heart allografts alone or heart and kidney allografts fr

46 ts show that low dose CO inhalation protects heart allografts and can considerably prolong their surv

47 (-/-) (H-2(b)) mice received B10.BR (H-2(k)) heart allografts and repeated doses of IgG2a, IgG1 or F(

48 in antibody-mediated chronic vasculopathy in heart allografts and the requirement for NK cell activat

49 e or chronic rejection of kidney, liver, and heart allografts and with development of allograft fibro

50 nd tofacitinib induced long-term survival of heart allografts and, importantly, it was equally effect

51 ction enhances the development of TVS in rat heart allografts, and this process is initiated between

52 ymphocytes, we found that newly transplanted heart allografts are rejected acutely, while healed-in a

53 th donor-specific primary liver, kidney, and heart allografts are significantly lower than rejection

54 at TLOs develop within chronically rejecting heart allografts, are predominantly B cell in origin, an

55 DBA/2J kidney allografts, but not heart allografts, are spontaneously accepted indefinitel

56 I (RT1a) rats reject Wistar-Furth (WF; RT1u) heart allografts at a mean survival time of 8.9+/-1.0 da

57 nt recipients rejected MHC class II-mismatch heart allografts at a much faster rate and showed a high

58 on of donation after circulatory death (DCD) heart allografts but has introduced complexity in the pr

59 -Ig induced long-term survival for wild-type heart allografts but not for CX3CR1(-/-) heart allograft

60 ACI recipients were rendered tolerant to WF heart allografts by a single injection via the portal ve

61 uce acceptance of heterotopic FVB/N (H-2(q)) heart allografts by C57BL/6 (H-2(b)) mice.

62 of single class II MHC-disparate B6.H-2bm12 heart allografts by C57BL/6 recipients is inhibited by t

63 sms preventing acute rejection of B6.H-2bm12 heart allografts by C57BL/6 recipients were investigated

64 e have successfully induced tolerance to rat heart allografts by recipient pretreatment with a single

65 donor-specific acceptance of rejection-prone heart allografts by recipients pretreated with immature

66 ronic allograft vasculopathy (CAV) in murine heart allografts can be elicited by adoptive transfer of

67 or ability to cause complement deposition in heart allografts compared with Abs induced by Th1 cells,

68 ted by day 10-14 posttransplant, while FVB/N heart allografts continued to function in C57BL/6, BCKO,

69 ression levels of several chemokine genes in heart allografts correlate with histologic rejection gra

70 splanted; however, long-term survival of ACI heart allografts could be induced when heart transplants

71 nti-thymocyte globulin (ATG)-lymphodepleted, heart-allografted cynomolgus monkeys.

72 SB allografts (day 38, NI=27 vs. 52) and the heart allografts (day 45, NI=43 vs. 83).

73 erse effect on the survival of the first LEW heart allografts, demonstrating the specificity of the t

74 ng regimen failed to induce tolerance to the heart allografts despite the development of mixed chimer

75 e exposed to NIMA accepted permanently K(b+) heart allografts despite the presence of normal levels o

76 Untreated PVG recipients of BN heart allografts displayed activation of both interleuki

77 sed expression of T-cell chemoattractants in heart allografts during later rejection when compared wi

78 Using transgenic mice as donors of heart allografts enabled us to monitor trafficking of do

79 ast colonies (55 of 85) isolated from female heart allografts expressed the male sry gene.

80 Tolerant ACI recipients bearing primary WF heart allografts for more than 100 days accepted second

81 but not third-party Brown Norway (BN; RT1n), heart allografts from 5.9 +/- 0.5 days in controls to 4.

82 tly increased the median survival time of BN heart allografts from 7 to 18-22 days.

83 hearts contained fewer dendritic cells, and heart allografts from CX3CR1(-/-) donors survived signif

84 Heart allografts from MHC-mismatched donors were transpl

85 iming and function of T cells in response to heart allografts from MHC-mismatched wild-type vs ICAM-1

86 examined the gene expression profiles of rat heart allografts from recipients treated with or without

87 art and kidney-heart transplants may protect heart allografts from rejection.

88 with allografts from STAT5a/b+/+ recipients, heart allografts from STAT5a/b-/- recipients had markedl

89 sed and computerized measurements performed, heart allografts from tolerant recipients showed signifi

90 Compared with heart allografts from WT mice, Tim4-/- heart allografts

91 C3H recipients of B10 heart allografts given perioperative B10 BM and tacrolim

92 grafts (H-2d) were accepted, and third-party heart allografts (H-2k) were rejected by tolerant PKCthe

93 of heart allografts showed that tolerant BN heart allografts had no evidence of acute or chronic rej

94 ) and PI3Kdelta (D910A/D910A) mice receiving heart allografts have suppression of alloreactive T effe

95 In 55-day heart allografts, IFN-gamma deficiency resulted in a sig

96 term graft survivors rejected third-party BN heart allografts in 14 days without an adverse effect on

97 a protein induced permanent acceptance of WF heart allografts in 16 of 26 ACI recipients (>100 days);

98 120 mg/kg PNU156804 extended the survival of heart allografts in a dose-dependent fashion.

99 heterotopically transplanted Lewis (RT1(l)) heart allografts in ACI (RT1(a)) recipients.

100 duces tolerance of Wistar Furth (WF; RT1.Au) heart allografts in ACI (RT1.Aa) recipients.

101 -69-RT1.Aa only prolonged the survival of WF heart allografts in ACI hosts (14.0+/-0.8 days; P<0.01).

102 nor blood cells facilitates tolerance to ACI heart allografts in Lewis rat hosts given posttransplant

103 blood cell infusion induce tolerance to ACI heart allografts in Lewis rat hosts.

104 r blood transfusion induced tolerance to ACI heart allografts in Lewis rats.

105 antigen presenting cells in the rejection of heart allografts in mice and differences among B7KO and

106 7359) on T-cell function and the survival of heart allografts in mice.

107 -specific tolerance induced by liver but not heart allografts in mice.

108 ages-avid nanoparticles detects rejection of heart allografts in mice.

109 nduced tolerance to Brown Norway (BN) (RT1n) heart allografts in PVG (RT1c) recipients more effective

110 al of RT1.Aa-disparate PVG.R8 (RT1.AaDuBuCu) heart allografts in PVG.1U (RT1u) hosts from 6.3 +/- 0.5

111 in allografts in naive recipients as well as heart allografts in skin-sensitized recipients.

112 nvestigated whether the long survival of the heart allografts in the pretreated mice was associated w

113 Survival of the rejection-prone heart allografts in the same strain combination is modes

114 s involves clonal deletion, and tolerance to heart allografts in this model also involves regulatory

115 hypothesis, we compared survival of skin and heart allografts in wild-type (IFN-gamma+/+) mice to tha

116 SRL produced dose-dependent prolongation of heart allografts: in untreated controls, 0.5 mg/kg SRL p

117 ecent transcriptome analysis of CMV-infected heart allografts indicates that the virus induces cytoki

118 B6.H-2bm12 heart allografts induced low levels of alloreactive effe

119 hich cotransplantation of a donor kidney and heart allograft induces tolerance to both organs in mini

120 bute to the lack of coronary arteriopathy in hearts allografted into GKO mice.

121 Transplant vasculopathy in kidney and heart allografts is associated with marked elevation of

122 es and continued acceptance of FVB/N-matched heart allografts is independent of host CD8+ T cells and

123 migration of donor leukocytes out of skin or heart allografts is not necessary for B or T cell allose

124 nt of luciferase activity in tissues (native heart, allograft, liver etc.) obtained post-transplant d

125 like cell lines, and immunostaining in human heart allografts localized the AIF-1 gene product to a s

126 body-mediated rejection (AMR) contributes to heart allograft loss.

127 F rats to reject in rapid fashion either LEW heart allografts (mean survival time [MST] = 4.2+/-0.4 d

128 s in the rigorous, nonprimarily vascularized heart allograft model in mice.

129 rotocol into the acute Wistar-Furth to Lewis heart allograft model resulted in a mean graft survival

130 The heterotopic heart allograft model using Brown Norway donors and Lewi

131 In a rat heart allograft model, preventing T cell costimulation w

132 ed into C57BL/6 mice that had accepted FVB/N heart allografts more than 60 days (heart acceptor mice)

133 Successful normothermic machine perfusion of heart allografts (MPH) has led to rapid growth in transp

134 The survival of both ACI heart allografts (MST=25.0 days, n=4) and small bowel al

135 . 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

136 ved either an isolated MHC class I disparate heart allograft (n=3) or combined class I disparate hear

137 recipients bearing either class I disparate heart allografts (n=5) or heart and kidney allografts (n

138 ive cells were not seen in the OLTx group of heart allografts nor in syngrafts.

139 dence that chronic rejection of vascularized heart allografts occurs in the complete absence of antib

140 ematopoietic chimeras then accepted skin and heart allografts of the same donor.

141 D-1 blockade led to accelerated rejection of heart allografts only in CD28(-/-) and CD8(-/-)CD28(-/-)

142 e showed a 4-fold increased survival time of heart allografts (p < 0.01).

143 vascularized and functional donor thymus to heart allograft recipients at the time of transplantatio

144 st to kidney allograft recipients, long-term heart allograft recipients eventually developed humoral

145 vo viral-gene expression in tissues from rat heart allograft recipients is highly restricted.

146 the donor-specific Ab produced in CCR5(-/-) heart allograft recipients is sufficient to directly med

147 sttransplant antidonor HLA antibodies in 168 heart allograft recipients transplanted from October 200

148 ly established that T cell recovery in mouse heart allograft recipients treated with anti-thymocyte g

149 ) expression is up-regulated in B cells from heart allograft recipients treated with murine anti-thym

150 similar regimens have proven unsuccessful in heart allograft recipients unless a kidney transplant wa

151 tivity in grafts and spleens of vascularized heart allograft recipients was also assessed.

152 ll help is not limited to the use of mATG in heart allograft recipients, and it is observed in nontra

153 In the heart allograft recipients, lower plasma LDH levels were

154 selective depletion of follicular B cells in heart allograft recipients, MZ B cells are sufficient fo

155 responses to the donor in a population of 34 heart allograft recipients.

156 subsets of donor-reactive memory Th cells as heart allograft recipients.

157 c indicators of T-CAD in a population of 274 heart allograft recipients.

158 nhanced Th1- or Th2-type immune responses of heart allograft recipients.

159 r-specific kidney is cotransplanted with the heart allograft, recipients become tolerant to donor ant

160 mplementation of a PA-led recovery model for heart allograft recovery showed no significant differenc

161 lockade of CSE with propargylglycine delayed heart allograft rejection and abrogated type IV hypersen

162 an recovery resulted in markedly accelerated heart allograft rejection and augmented host effector an

163 re we analyzed the role of mouse IgV-CD80 in heart allograft rejection and search for equivalent spli

164 or-derived dendritic cells resulted in acute heart allograft rejection by 4C T cells, demonstrating t

165 investigate the role of macrophages in acute heart allograft rejection by cellular and functional MRI

166 ers of IgG alloantibodies that contribute to heart allograft rejection in CD40-/- heart recipients.

167 ted but only delayed CD4+/CD8+ Teff-mediated heart allograft rejection in Rag-/- mice.

168 fective at constraining B cell responses and heart allograft rejection in sensitized recipients.

169 Acute heart allograft rejection occurred at the same tempo in

170 ther indirect allorecognition is involved in heart allograft rejection T cells obtained from peripher

171 rred to Rag1-/- recipients failed to mediate heart allograft rejection until supplemented with STAT5a

172 o mediate T cell reconstitution and initiate heart allograft rejection upon adoptive transfer into mA

173 Heart allograft rejection was less common in heart-kidne

174 Although Mig antagonism delays acute heart allograft rejection, the results also suggest that

175 lloimmunity, as evidenced by acceleration of heart allograft rejection.

176 S) beyond 0.06 x 10(9)/liter precede treated heart allograft rejection.

177 ules blocks memory and attenuates kidney and heart allograft rejection.

178 l to effector T cells and APCs, accelerating heart allograft rejection.

179 Histology of heart allografts showed that tolerant BN heart allograft

180 ivate more H-2K(b)-specific T cells in vivo; heart allografts stimulate the activation and proliferat

181 othelial venules) were detectable in 9 of 13 heart allografts studied and were predominantly B cell i

182 /6 recipients of fully MHC-mismatched BALB/c heart allografts, suggesting the possible generation of

183 T cell-specific pan-Notch blockade prolonged heart allograft survival and decreased IFN-gamma and IL-

184 Mean heart allograft survival as evaluated by daily abdominal

185 h a small molecule inhibitor prolongs murine heart allograft survival at least partially through dimi

186 ndirect pathway T-cell responses and prolong heart allograft survival but fail to directly regulate T

187 Here, we investigated whether long-term heart allograft survival could be achieved by cotranspla

188 t of B7 costimulation blockade in prolonging heart allograft survival in a major histocompatibility c

189 0.05-8.0 mg/kg/day) by oral gavage prolonged heart allograft survival in dose-dependent fashion.

190 mulation pathways induces long-term skin and heart allograft survival in IFN-gamma+/+ recipients but

191 ere tested for their capacity to prolong ACI heart allograft survival in Lewis hosts.

192 d hematopoietic chimerism leads to long-term heart allograft survival in MHC disparate monkeys withou

193 regulatory T cell development and long-term heart allograft survival in recipients treated with peri

194 y T cell expansion and significantly extends heart allograft survival in sensitized recipients.

195 mouse (m) IL-10 on heterotopic vascularized heart allograft survival in the B10(H2b)-->C3H(H2k) stra

196 r, were tested for their capacity to prolong heart allograft survival in this model.

197 bited cytotoxic cells in vitro and prolonged heart allograft survival in vivo.

198 icity, binding to hsc70, and prolongation of heart allograft survival in vivo.

199 he ME C-raf antisense oligos produced better heart allograft survival rates than did PS C-raf oligo.

200 l antidonor T cell responses, and prolonging heart allograft survival than the commonly used treatmen

201 D40, CD80, CD86)-deficient can prolong mouse heart allograft survival This is associated with microch

202 T1.Aa-Sf9 or ms/RT1.Aa-Sf9 cells reduced ACI heart allograft survival to 3.8 +/- 0.4 days or 3.7 +/-

203 -100) was remarkably effective in prolonging heart allograft survival to a median of >100 from 45 day

204 This marked increase in heart allograft survival was associated with reduced ant

205 Long-term, immunosuppression-free heart allograft survival was consistently achieved in he

206 nd the influence of renal DC on vascularized heart allograft survival was determined.

207 In both groups the median heart allograft survival was similar at around 26 days.

208 in rhesus monkeys would cause: (1) prolonged heart allograft survival, (2) inhibition of primary but

209 C-raf inhibition extends heart allograft survival, and ME-modification potentiate

210 f oral SRL and CsA synergistically prolonged heart allograft survival, as documented by combination i

211 olimus (SRL) acted synergistically to extend heart allograft survival, the effect was potentiated by

212 ells at the time of transplant prolonged C3H heart allograft survival, whereas FL-BM cells did not.

213 ls, recombinant EPO administration prolonged heart allograft survival, whereas pharmacologic downregu

214 transplant recipients resulted in long-term heart allograft survival, which was associated with dimi

215 -mismatched (C3HHeJ; C3H(H-2k)) vascularized heart allograft survival, with long-term (>100 days) don

216 inhibition of C-raf mRNA expression prolongs heart allograft survival.

217 ecipients exhibit indefinite prolongation of heart allograft survival.

218 ti-CD154-induced prolongation of CX3CR1(-/-) heart allograft survival.

219 hened the effect of anti-CD40L in prolonging heart allograft survival.

220 ciency offered only marginal prolongation of heart allograft survival.

221 cute graft-versus-host disease and prolonged heart allograft survival; peripheral CD8 T-cell depletio

222 ccurred by day 10 posttransplant, while most heart allografts survived for more than 60 days.

223 with heart allografts from WT mice, Tim4-/- heart allografts survived much longer and were more easi

224 nscriptional decrease in FOXO1 expression in heart allografts that is localized to both the cardiomyo

225 that CD8 T-cell-mediated rejection of murine heart allografts that lack hematopoietic APCs requires h

226 ntibodies and chronic rejection of kidney or heart allografts, the clinical significance of anti-HLA

227 f animals bearing isolated class I disparate heart allografts, the thymectomized recipients rejected

228 cells triggered acute rejection of wild-type heart allografts, they failed to trigger rejection of GR

229 destruction of passenger lymphocytes within heart allografts, this process occurs too slowly to prev

230 ted with tacrolimus plus ortho IL-2 achieved heart allograft tolerance, even after tacrolimus cessati

231 allograft injury, we tested the rejection of heart allografts transgenically expressing a single clas

232 Here the author show, using mouse heart allograft transplantation models, that PI3Kgamma o

233 of syngeneic grafts and ACI recipients of WF heart allografts treated with high-dose CsA (10 mg/kg/da

234 ewis (LEW) liver, bone marrow cell (BMC) and heart allografts under a brief course of tacrolimus.

235 Lewis rats were rendered tolerant to ACI heart allografts using a regimen of posttransplant total

236 The second ACI heart allograft was permanently accepted by tolerant Lew

237 Indeed, survival of the heart allografts was dependent on lymphatic drainage fro

238 sponses in the absence of CD28, rejection of heart allografts was studied in CD28-deficient mice.

239 fected COS7 cell cultures and in transfected heart allografts were examined by enzyme immunoassay (EI

240 Heart allografts were rejected at an accelerated rate in

241 Wild-type C57BL/6 (H-2(b)) heart allografts were rejected by A/J (H-2(a)) recipient

242 cepted, whereas third-party (Sprague-Dawley) heart allografts were rejected by the tolerant recipient

243 Unlike kidney allografts, heart allografts were rejected in 33-55 days.

244 In the present study, heart allografts were transplanted across the same MHC c

245 When FVB/N hepatocytes and heart allografts were transplanted into C57BL/6 or BCKO

246 Fully MHC-mismatched heart allografts were transplanted into three groups of

247 d second heart or third-party (Brown Norway) heart allografts were transplanted.

248 urth (RT1u) rat recipients of Buffalo (RT1b) heart allografts were treated with FTY720 alone or in co

249 ients of heterotopic vascularized B10 (H-2b) heart allografts were treated with recombinant (r) mouse

250 Recipients with long-term-surviving heart allografts were unable to reject B6.H-2bm12 skin a

251 or histocompatibility-mismatched donor mouse heart allografts with alloimmune-mediated vasculopathy u

252 nduce a similar survival of Brown Norway rat heart allografts with an equal suppression of intragraft

253 fector functions following infiltration into heart allografts with low or high intensities of ischemi

254 osts rejected allo-mismatched WT or CD40L-/- heart allografts within 2 wk.