ライフサイエンスコーパス: cardiac allograft

1 t the development of arteriosclerosis in rat cardiac allograft.

2 t induces H4 immunodominance in vascularized cardiac allograft.

3 nts have had no evidence of amyloid in their cardiac allograft.

4 gene delivery and expression isolated to the cardiac allograft.

5 tion of LVH and diastolic dysfunction of the cardiac allograft.

6 neficial effect on allograft survival in rat cardiac allografts.

7 on and promote tolerance induction to murine cardiac allografts.

8 fectively prolonged the survival time of rat cardiac allografts.

9 active in T cells that infiltrate and reject cardiac allografts.

10 histocompatibility complex (MHC)-mismatched cardiac allografts.

11 cynomolgus monkey recipients of heterotopic cardiac allografts.

12 ansfer of donor MHCII genes in recipients of cardiac allografts.

13 athways, as was histological analysis of the cardiac allografts.

14 D154-mediated acceptance of fully mismatched cardiac allografts.

15 to C57BL/6 mice that received alloantigen or cardiac allografts.

16 l of fully MHC-mismatched vascularized mouse cardiac allografts.

17 rendered these recipients able to reject A/J cardiac allografts.

18 ansferred into Rag2 -/- mice with or without cardiac allografts.

19 e activity and induced long-term survival of cardiac allografts.

20 bility of B6.muMT(-/-) CD4 T cells to reject cardiac allografts.

21 protein (SA-FasL) for tolerance induction to cardiac allografts.

22 tolerance to donor, but not F344 third-party cardiac allografts.

23 ansplants continues to limit the survival of cardiac allografts.

24 Ab and prevents macrophage infiltration into cardiac allografts.

25 rmation and exacerbates chronic rejection in cardiac allografts.

26 cial actions determines the final outcome of cardiac allografts.

27 -mismatched skin and MHC class II-mismatched cardiac allografts.

28 e::IL-10) mice, received vascularized BALB/c cardiac allografts.

29 diac troponin T release in the rat and mouse cardiac allografts 6 hours after reperfusion, respective

30 demonstrate that stimulating OX40 overrides cardiac allograft acceptance induced by disrupting CD40-

31 CTLA4-Ig to promote long-term acceptance of cardiac allografts across a major histocompatibility bar

32 might be a useful therapy that could protect cardiac allografts against CAV.

33 1-/- hosts bearing donor-type or third-party cardiac allografts and by regulatory T-cell depletion wi

34 anti-ER-TR7 mice received BALB/c heterotopic cardiac allografts and graft survival was monitored.

35 182 was significantly increased in rejecting cardiac allografts and in mononuclear cells that infiltr

36 of donor ECDI-SPs in protecting vascularized cardiac allografts and mechanism(s) of protection are un

37 ue to AMR compared with that of nonrejecting cardiac allografts and native hearts.

38 nd quantify Du51-specific T cells within rat cardiac allografts and spleen.

39 (-/-) mice underlies the inability to reject cardiac allografts and this inability is overcome by div

40 accumulation of CD11b(+) IDO(+) cells in the cardiac allograft, and that the presence of this populat

41 o long-term survival of fully MHC-mismatched cardiac allografts, and prevented development of transpl

42 Also, KO recipients of fully MHC-mismatched cardiac allografts are resistant to the graft-prolonging

43 finding that was maintained in the accepted cardiac allografts at d100.

44 Bcl-2 and preserved capillary density in rat cardiac allografts at day 10.

45 ed on CD3(+) T cell infiltrates within human cardiac allograft biopsies with evidence of rejection.

46 In cardiac allograft biopsies with immunopathologic AMR, IR

47 immunoregulatory and promote engraftment of cardiac allografts, but their influence is diminished by

48 lts demonstrate that the direct rejection of cardiac allografts by CD4 effector T cells requires the

49 onic liposome (GAP/DLRIE) was delivered into cardiac allografts by intracoronary infusion ex vivo.

50 alone was unable to inhibit the rejection of cardiac allografts by wild-type recipients.

51 responses and prolonging the survival of old cardiac allografts comparable to young donor organs.

52 We used PKCtheta mice as recipients of cardiac allografts, compared with wild-type (WT) cardiac

53 L may be useful to attenuate LVH and improve cardiac allograft diastolic function.

54 xpression of Ang-1 fails to protect from rat cardiac allograft due to smooth muscle cell activation.

55 Forty-six percent had persistent cardiac allograft dysfunction.

56 from 12 failing native hearts and 2 rejected cardiac allografts explanted during transplant surgery.

57 ession therapy that prevent acute rejection, cardiac allografts fail at rates of 3% to 5% per posttra

58 opathy (CAV) is the preeminent cause of late cardiac allograft failure characterized histologically b

59 o more intensely and more frequently monitor cardiac allografts for rejection.

60 C57BL/6 (H-2) mice received vascularized cardiac allografts from A/J (H-2) donors and were treate

61 e B6 mice were transplanted with heterotopic cardiac allografts from allogeneic BALB/c donors.

62 ed at 1-hour posttransplant to recipients of cardiac allografts from CMV-infected donors significantl

63 promising approach for extending survival of cardiac allografts from CMV-infected donors.

64 We transplanted cardiac allografts from Dark Agouti rat and Balb mouse d

65 Using cardiac allografts from high-risk donors who are serolog

66 of any identified abnormalities in terms of cardiac allograft function and suitability for transplan

67 gnificant difference in cardiac rejection or cardiac allograft function.

68 Donor-type second cardiac allografts (H-2d) were accepted, and third-party

69 r delayed: d3-7) to mice transplanted with a cardiac allograft (H2(b)-to-H2(k); d0).

70 ns of B cell and plasma cell infiltration in cardiac allografts has not been documented.

71 ay inhibitor to prevent chronic rejection of cardiac allografts in a rat model.

72 Rejected MHC-mismatched cardiac allografts in CCR5(-/-) recipients have low T ce

73 r transplantation of vascularized kidney and cardiac allografts in mice.

74 e same therapy induced long-term survival of cardiac allografts in PKCtheta mice.

75 activity was also elevated in the wild-type cardiac allografts in Rag2 -/- mice that were transferre

76 T cell-mediated rejection of MHC-mismatched cardiac allografts in the absence of both CD8 T and B ly

77 Fifty-seven percent of potential cardiac allografts in this cohort were accepted for tran

78 Delta1 mAb only slightly delayed survival of cardiac allografts in this fully MHC-mismatched model, i

79 pression of IL-27 and TGF-beta1 in tolerated cardiac allografts in two different rodent models.

80 ll proliferation in vitro and traffic to the cardiac allografts in vivo to mediate their protection v

81 Cardiac allografts in young mice (2-3 months) treated wi

82 ell depletion from the BALB.B donor prior to cardiac allograft induces H4 immunodominance in vascular

83 circumvented tolerance induction and induced cardiac allograft inflammation and rejection in murine m

84 The hallmark of cardiac allograft injury is the infiltration of leukocyt

85 Heterotopic, abdominal transplantation of cardiac allografts into landrace or into Munich mini pig

86 est that CTLA4Ig-induced tolerance to murine cardiac allografts is critically dependent on synergisti

87 rgan donor is vasculoprotective and inhibits cardiac allograft ischemia-reperfusion injury.

88 Interestingly, non-primarily vascularized cardiac allografts mimicked skin grafts in the observed

89 match, as well as using a murine heterotopic cardiac allograft model (BALB/c->C57BL/6).

90 developed a donor-type skin-sensitized mouse cardiac allograft model (BALB/c-->C57BL/6) in which both

91 e developed a mouse vascularized heterotopic cardiac allograft model in which B6.RAG1 KO hosts (H-2K(

92 A murine long-term cardiac allograft model using immunosuppression (preoper

93 Additionally, in a rat cardiac allograft model, IL-34 potently induced transpla

94 In a murine cardiac allograft model, LTbRIg treatment reversed the t

95 ficiency in B cells prevented tolerance in a cardiac allograft model, resulting in rapid acute cardia

96 In the cardiac allograft model, the combination of transient mA

97 In the mouse vascularized cardiac allograft model, transient depletion of CD4(+) c

98 elop severe chronic arteriopathy in a murine cardiac allograft model.

99 aft survival in a full MHC-mismatched murine cardiac allograft model.

100 PD 167), in an established cynomolgus monkey cardiac allograft model.

101 induced by CTLA4Ig in a fully MHC-mismatched cardiac allograft model.

102 mismatched, BALB.B (H-2B) to C57BL/6 (H-2B), cardiac allograft model.

103 In ELP-/- cardiac allografts, mononuclear cell infiltration and va

104 -4 and IL-10 combined gene therapy protected cardiac allograft myocytes by down-regulating its FasL e

105 ive T-cell apoptosis or prevent apoptosis of cardiac allograft myocytes through Fas/Fas ligand (FasL)

106 Cardiac allografts of B6 major histocompatibility comple

107 We demonstrate that cardiac allografts of mice treated with anti-MHC class I

108 ed to prevent accumulation of CD4 T cells in cardiac allografts of sensitized recipients.

109 Current regulations require that all cardiac allograft offers for transplantation must includ

110 ens are still associated with poor long-term cardiac allograft outcomes, and with the development of

111 immune and non-immune factors affecting late cardiac allograft outcomes.

112 In mouse cardiac allografts PDGF receptor-beta, but not -alpha in

113 A/J (H-2(a)) cardiac allografts placed into wild-type BALB/c (H-2(d))

114 anded following transplantation, migrated to cardiac allografts, prolonged graft survival, and were s

115 inal sera from a multicenter cohort of adult cardiac allograft recipients (samples: n = 477 no reject

116 ll crossmatch-positive sera obtained from 12 cardiac allograft recipients at the time of biopsy-prove

117 Histology in FcgammaRIII-KO cardiac allograft recipients indicated perivascular marg

118 f T. gondii infection on survival of our 582 cardiac allograft recipients operated upon between June

119 Antibody-mediated rejection (AMR) in cardiac allograft recipients remains less well-understoo

120 Cynomolgus monkey heterotopic cardiac allograft recipients were treated with either ID

121 d IGFPB-3 might be beneficial in identifying cardiac allograft recipients who are prone to develop CA

122 We hypothesized that viral infection of the cardiac allograft reduces graft survival.

123 Freedom from cardiac allograft rejection (ISHLT > or =grade 2) for CH

124 cells play a critical role in initiation of cardiac allograft rejection and allograft vasculopathy.

125 is an important risk factor for accelerated cardiac allograft rejection and graft dysfunction .

126 It effectively diminishes acute cardiac allograft rejection and is suitable for combinat

127 e activation of NF-kappaB signaling in mouse cardiac allograft rejection and ischemia-reperfusion inj

128 of nuclear factor (NF)-kappaB activation in cardiac allograft rejection and ischemia-reperfusion inj

129 nd, we neutralized IL-6 in settings of acute cardiac allograft rejection associated with either CD8(+

130 xamined in murine models of acute or chronic cardiac allograft rejection by transplanting recipients

131 The changing epidemiology of cardiac allograft rejection has prompted many to questio

132 Moreover, cardiac allograft rejection in HFD mice was modestly acc

133 In our model of fulminant cardiac allograft rejection in sensitized hosts, groups

134 not PDL2 blockade significantly accelerated cardiac allograft rejection in the bm12-into-B6 and B6-i

135 TLA4-Ig, which was not sufficient to prevent cardiac allograft rejection in the wild-type mice, preve

136 ted survival is required for T cell-mediated cardiac allograft rejection in this adoptive transfer mo

137 ribution of recipient macrophages in chronic cardiac allograft rejection in vivo.

138 al antibody or human CTLA4Ig failed to delay cardiac allograft rejection in WT mice, the same therapy

139 phagocytosis or protease activity can detect cardiac allograft rejection noninvasively, promise to en

140 Acute cardiac allograft rejection requires host, but not donor

141 and recipient selectins in acute and chronic cardiac allograft rejection using mice deficient in all

142 s study investigated the role of MRP-8/14 in cardiac allograft rejection using MRP-14(-/-) mice that

143 by the absence of IL-17, and the kinetics of cardiac allograft rejection were similar in wild-type an

144 B cell depletion did not affect acute cardiac allograft rejection, although CD19 mAb treatment

145 cate that macrophages are essential in acute cardiac allograft rejection, and selective depletion of

146 nd class I-mismatched models of vascularized cardiac allograft rejection, blocking anti-PDL1 and anti

147 pients of bm12 allografts led to accelerated cardiac allograft rejection, despite similar mean BP and

148 ansplantations were performed to study acute cardiac allograft rejection, graft survival, suppression

149 C-theta-/- T cells was sufficient to restore cardiac allograft rejection, suggesting that PKC-theta-r

150 ta-/- mice displayed delayed, but successful cardiac allograft rejection, suggesting the potential co

151 complement activation leading to accelerated cardiac allograft rejection.

152 after renal ischemia reperfusion injury and cardiac allograft rejection.

153 istocompatibility complex (MHC)-incompatible cardiac allograft rejection.

154 l target for novel therapeutic treatment for cardiac allograft rejection.

155 ing IL-6 should be considered for preventing cardiac allograft rejection.

156 e as effector cells to mediate primary acute cardiac allograft rejection.

157 brogated the ability of CpG to promote acute cardiac allograft rejection.

158 human DAF) deficiency on CD8 T cell-mediated cardiac allograft rejection.

159 ents did not exhibit an accelerated tempo of cardiac allograft rejection.

160 n of Bcl-xL is essential for T cell-mediated cardiac allograft rejection.

161 lymphocyte reaction and in vivo by targeting cardiac allograft rejection.

162 med to establish the role of RIP3 in chronic cardiac allograft rejection.

163 ac allograft model, resulting in rapid acute cardiac allograft rejection.

164 Equitable allocation of cardiac allografts requires further investigation of the

165 ne transfer and neutralization of TGFbeta in cardiac allografts significantly attenuated interstitial

166 nfirmed that the protein is present in human cardiac allograft specimens undergoing acute graft rejec

167 ction and immunomodulation during IRI in rat cardiac allografts subjected to prolonged ischemia time.

168 nses to alloantigens, and produced long-term cardiac allograft survival (>100 days) in 10 out of 11 r

169 ses of R348 or rapamycin for 5 days; and (4) cardiac allograft survival after a 10-day treatment peri

170 CAV is the most important determinant of cardiac allograft survival and a major cause of death af

171 erm immunosuppression allows prolongation of cardiac allograft survival and one tolerant recipient.

172 the allo-immune responses and prolonged the cardiac allograft survival by 15 folds.

173 xidative stress, reduces posttransplantation cardiac allograft survival by 33% to 57%, and increases

174 infusions of ECDI-SPs significantly prolong cardiac allograft survival concomitant with an impressiv

175 chymal rejection and significantly prolonged cardiac allograft survival from 8.3+/-1.3 days in WT rec

176 hort course of rapamycin provides indefinite cardiac allograft survival in 100% of the recipients.

177 Donor-derived MDSCs prolong cardiac allograft survival in a donor-specific manner vi

178 ole of Tregs expanded in vivo by TNFRSF25 on cardiac allograft survival in a mouse model of fully maj

179 ion between CD40 and CD40L induces long-term cardiac allograft survival in rats through a CD8+CD45RCl

180 unction was insufficient to markedly prolong cardiac allograft survival in sensitized BKO recipients.

181 lockade promotes significant prolongation of cardiac allograft survival in wild-type but not in CD8-d

182 (VDR) impacts costimulatory blockade induced cardiac allograft survival is not known.

183 In vivo, fully MHC mismatched cardiac allograft survival is significantly prolonged in

184 Costimulatory blockade-induced murine cardiac allograft survival requires intragraft accumulat

185 eutralization of IL-17 facilitates long-term cardiac allograft survival with combined T cell co-stimu

186 Foxp3(+) Tregs that underlie IL-33-mediated cardiac allograft survival.

187 ll molecule inhibitor, AMG1237845, in murine cardiac allograft survival.

188 he effects of rIFN-gamma infusion on porcine cardiac allograft survival.

189 Although wild-type cardiac allografts survived long term, PDL1-/- donor hea

190 We previously demonstrated in a rat model of cardiac allograft tolerance induced by short-term immuno

191 GF)-beta1 as overexpressed in a model of rat cardiac allograft tolerance mediated by regulatory CD4CD

192 cell surface interaction, therefore inducing cardiac allograft tolerance.

193 demonstrating full reconstitution and donor cardiac-allograft tolerance and no GVHD with expanded do

194 iac allografts, compared with wild-type (WT) cardiac allograft transplantation.

195 gators showing fewer rejections in renal and cardiac allografts transplanted into recipients with hig

196 Indeed, cardiac allografts underwent fulminant rejection in sens

197 sociations between specific ECG findings and cardiac allograft use for transplantation were studied.

198 letion to modulate alloimmunity or attenuate cardiac allograft vasculopathy (CAV) (classic chronic re

199 acute antibody-mediated rejection (AMR) and cardiac allograft vasculopathy (CAV) after human heart t

200 e evaluated the association between Lp-PLA2, cardiac allograft vasculopathy (CAV) assessed by 3D intr

201 Cardiac allograft vasculopathy (CAV) has a high prevalen

202 Cardiac allograft vasculopathy (CAV) has an incidence of

203 tomography angiography (CCTA) for detecting cardiac allograft vasculopathy (CAV) in comparison with

204 Cardiac allograft vasculopathy (CAV) is a major cause of

205 Cardiac allograft vasculopathy (CAV) is a major contribu

206 Cardiac allograft vasculopathy (CAV) is a major limitati

207 Cardiac allograft vasculopathy (CAV) is an increasingly

208 Cardiac allograft vasculopathy (CAV) is associated with

209 Cardiac allograft vasculopathy (CAV) is the main cause o

210 Because cardiac allograft vasculopathy (CAV) is the major cause

211 Cardiac allograft vasculopathy (CAV) is the preeminent c

212 Cardiac allograft vasculopathy (CAV) is the principal ca

213 Although cardiac allograft vasculopathy (CAV) is typically charac

214 hy has been clearly established, its role in cardiac allograft vasculopathy (CAV) is unclear.

215 el wall inflammation and its significance in cardiac allograft vasculopathy (CAV) progression.

216 Cardiac allograft vasculopathy (CAV) remains a leading c

217 Cardiac allograft vasculopathy (CAV) remains the Achille

218 Cardiac allograft vasculopathy (CAV) remains the leading

219 cular magnetic resonance (CMR) for detecting cardiac allograft vasculopathy (CAV) using contemporary

220 Cardiac allograft vasculopathy (CAV) was graduated in ac

221 A role for natural killer (NK) cells in cardiac allograft vasculopathy (CAV) was suggested by ou

222 between cytomegalovirus (CMV) infection and cardiac allograft vasculopathy (CAV) were conducted on p

223 between cytomegalovirus (CMV) infection and cardiac allograft vasculopathy (CAV) were conducted on p

224 on the initial TTE for recipient mortality, cardiac allograft vasculopathy (CAV), and primary graft

225 ages of this approach include attenuation of cardiac allograft vasculopathy (CAV), improvement in glo

226 t 1 year after HTx and future development of cardiac allograft vasculopathy (CAV).

227 l homeostasis may prevent the development of cardiac allograft vasculopathy (CAV).

228 art is a central event in the development of cardiac allograft vasculopathy (CAV).

229 pressures to augment angiographic grading of cardiac allograft vasculopathy (CAV); however, no data e

230 -segment-elevation myocardial infarction and cardiac allograft vasculopathy after heart transplantati

231 se include a higher risk of acute rejection, cardiac allograft vasculopathy after heart transplantati

232 er transplantation, may increase the risk of cardiac allograft vasculopathy and allograft loss, but n

233 Understanding of the mechanisms surrounding cardiac allograft vasculopathy and insight into the poss

234 ion and risk stratification of patients with cardiac allograft vasculopathy are problematic.

235 oronary IVUS data show that H+LTx attenuates cardiac allograft vasculopathy by decreasing the rate of

236 icacy to prolong graft survival and to delay cardiac allograft vasculopathy development and antidonor

237 ngation of graft survival and suppression of cardiac allograft vasculopathy development.

238 ts prevalence was positively associated with cardiac allograft vasculopathy grade.

239 4C T cells caused cardiac allograft vasculopathy in the absence of other T

240 Cardiac allograft vasculopathy is a key prognostic deter

241 Cardiac allograft vasculopathy is a multifactorial proce

242 Cardiac allograft vasculopathy is the major cause of lat

243 Cardiac allograft vasculopathy is the major limiting fac

244 rferon-gamma--producing T cells and enhanced cardiac allograft vasculopathy lesion formation.

245 Cardiac allograft vasculopathy lesions contain alloreact

246 imary immunosuppressant attenuates long-term cardiac allograft vasculopathy progression and may impro

247 ucing calcineurin inhibitor use, attenuating cardiac allograft vasculopathy progression and reducing

248 osuppressant in the long-term attenuation of cardiac allograft vasculopathy progression and the effec

249 SRL as primary immunosuppression attenuates cardiac allograft vasculopathy progression.

250 s a primary immunosuppressant in attenuating cardiac allograft vasculopathy progression.

251 hat is not fully explained by attenuation of cardiac allograft vasculopathy progression.

252 Cardiac allograft vasculopathy remains a major limiting

253 Cardiac transplant arteriosclerosis or cardiac allograft vasculopathy remains the leading cause

254 man SMC, and human arteriovenous fistula and cardiac allograft vasculopathy samples to assess the rol

255 timal hyperplastic arteriovenous fistula and cardiac allograft vasculopathy samples, and inversely co

256 IDEC-131-treated grafts had higher cardiac allograft vasculopathy severity scores during tr

257 study a mouse model of autoantibody-mediated cardiac allograft vasculopathy to clarify the alloimmune

258 Similarly, cardiac allograft vasculopathy up to 5 years and primary

259 tect the heart graft from the development of cardiac allograft vasculopathy using coronary three-dime

260 (Prevention of Cardiac Allograft Vasculopathy Using Rituximab [Rituxan]

261 The CTOT-11 (Prevention of Cardiac Allograft Vasculopathy Using Rituximab Therapy i

262 ted tomography angiography (CTA) to rule out cardiac allograft vasculopathy versus 16 patients withou

263 rular filtration rate, previously documented cardiac allograft vasculopathy), relative perfusion defe

264 ated by cohort for time until graft failure, cardiac allograft vasculopathy, and hospitalization for

265 ET-1 may also play a significant role in cardiac allograft vasculopathy, and in animal models, ER

266 delayed alloantibody production, suppressed cardiac allograft vasculopathy, and tended to further pr

267 Moreover, imatinib mesylate enhanced rat cardiac allograft vasculopathy, cardiac fibrosis, and la

268 Finally, in a murine model of cardiac allograft vasculopathy, depletion of donor CD4 n

269 myocardial fibrosis variables to models with cardiac allograft vasculopathy, history of rejection, ti

270 CI, 1.59-5.23; P<0.001) after adjustment for cardiac allograft vasculopathy, history of rejection, ti

271 associated with intermediate-term mortality, cardiac allograft vasculopathy, or primary graft failure

272 particular, by chronic rejection leading to cardiac allograft vasculopathy, remains a major cause of

273 reased graft survival and the development of cardiac allograft vasculopathy, suggesting a contributio

274 Cardiac allograft vasculopathy, the nature of the inflam

275 e incidence of primary graft dysfunction and cardiac allograft vasculopathy-free survival did not sig

276 arly posttransplant bleeding, rejection, and cardiac allograft vasculopathy-free survival.

277 ho have exhibited early onset or accelerated cardiac allograft vasculopathy.

278 eactive T cell activation and development of cardiac allograft vasculopathy.

279 pharmacotherapies to halt the progression of cardiac allograft vasculopathy.

280 No difference was found in deaths due to cardiac allograft vasculopathy.

281 modeling, may be an important determinant of cardiac allograft vasculopathy.

282 on and is associated with the development of cardiac allograft vasculopathy.

283 levels, which may in turn reduce the risk of cardiac allograft vasculopathy.

284 n therapy would attenuate the development of cardiac allograft vasculopathy.

285 gnificant risk factor for the development of cardiac allograft vasculopathy.

286 ely correlates with SMAD3 phosphorylation in cardiac allograft vasculopathy.

287 ting cellular trafficking, alloimmunity, and cardiac allograft vasculopathy.

288 ic rejection of MHC class II-mismatched bm12 cardiac allografts was accelerated in FcgammaRIIb(-/-) m

289 sitization phase, the fulminant rejection of cardiac allografts was B-cell-independent, and CD154 blo

290 In this study, gene transfer of decorin into cardiac allografts was used to assess the impact of intr

291 As expected, all cardiac allografts were acutely rejected.

292 , in which B6.RAG1(-/-) recipients of BALB/c cardiac allografts were passively transferred with donor

293 RAG1(-/-) recipients of BALB/c cardiac allografts were passively transferred with donor

294 Heterotopic donor C57BL/6 cardiac allografts were performed at day 243 after BMT.

295 Fully mismatched cardiac allografts were transplanted into alemtuzumab tr

296 activity was significantly increased in the cardiac allografts when NF-kappaB-Luc mice were used as

297 pe T cells readily rejected fully mismatched cardiac allografts, whereas Rag1-/- mice reconstituted w

298 emonstrated B cell clonal expansion in human cardiac allografts with CAV.

299 s and transplanted chimeras with heterotopic cardiac allografts with or without costimulatory blockad

300 Our results suggest that more liberal use of cardiac allografts with relative contraindications may b