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 tion of LVH and diastolic dysfunction of the cardiac allograft.

5 fectively prolonged the survival time of rat cardiac allografts.

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

7 histocompatibility complex (MHC)-mismatched cardiac allografts.

8 rmation and exacerbates chronic rejection in cardiac allografts.

9 cynomolgus monkey recipients of heterotopic cardiac allografts.

10 cial actions determines the final outcome of cardiac allografts.

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

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

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

14 D154-mediated acceptance of fully mismatched cardiac allografts.

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

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

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

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

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

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

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

22 ansplants continues to limit the survival of cardiac allografts.

23 in preventing CD28-independent rejection of cardiac allografts.

24 mice, tenascin-C-/- mice fail to vascularize cardiac allografts.

25 bystanders during rejection of MHC-disparate cardiac allografts.

26 ells essential for tolerance to vascularized cardiac allografts.

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

28 Ab and prevents macrophage infiltration into cardiac allografts.

29 neficial effect on allograft survival in rat cardiac allografts.

30 on and promote tolerance induction to murine cardiac allografts.

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

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

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

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

35 morphological lesion of chronically failing cardiac allografts, also seen in chronic renal and liver

36 1-/- hosts bearing donor-type or third-party cardiac allografts and by regulatory T-cell depletion wi

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

38 182 was significantly increased in rejecting cardiac allografts and in mononuclear cells that infiltr

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

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

41 lls prolonged survival of murine heterotopic cardiac allografts and synergizes with conventional cost

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

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

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

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

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

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

48 that B7-deficient hosts do not simply ignore cardiac allografts, but rather spontaneously develop tra

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

50 zation caused accelerated acute rejection of cardiac allografts by C6-sufficient recipients (4 days).

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

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

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

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

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

56 How subclinical viral replication influences cardiac allograft disease remains poorly understood, as

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

58 Forty-six percent had persistent cardiac allograft dysfunction.

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

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

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

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

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

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

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

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

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

68 gnificant difference in cardiac rejection or cardiac allograft function.

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

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

71 CR5(-/-) (H-2(b)) recipients of A/J (H-2(a)) cardiac allografts had equivalent numbers of donor-react

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

73 CD154-based tolerance induction for primate cardiac allografts have not previously been defined.

74 Cardiac allograft hypertrophy is associated with persist

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

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

77 long-term acceptance of fully MHC-mismatched cardiac allografts in large animals.

78 Cardiac allografts in MCP-1-/- recipients survived signi

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

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

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

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

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

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

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

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

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

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

89 es that determine the balance between active cardiac allograft injury and repair.

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

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

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

93 initially identified in chronically rejected cardiac allografts, may be involved in the pathogenesis

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

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

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

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

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

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

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

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

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

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

104 Using a murine cardiac allograft model, we recently demonstrated that t

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

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

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

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

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

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

111 -4 and IL-10 combined gene therapy protected cardiac allograft myocytes by down-regulating its FasL e

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

113 Cardiac allografts of B6 major histocompatibility comple

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

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

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

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

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

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

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

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

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

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

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

125 CD8 CTL effectors in CD4 knockout (KO) skin/cardiac allograft recipients.

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

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

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

129 5/Fc fusion protein is sufficient to prevent cardiac allograft rejection and induce antigen-specific

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

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

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

133 transplantation by T-cell immunity may limit cardiac allograft rejection and vascular disease.

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

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

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

137 at B7-deficient T-cells are capable of acute cardiac allograft rejection in a B7-replete environment.

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

139 ipients, and transfer of this serum provoked cardiac allograft rejection in RAG-1(-/-) recipients wit

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

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

142 bsence of decay-accelerating factor (DAF) on cardiac allograft rejection in the presence of different

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

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

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

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

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

148 Acute cardiac allograft rejection requires host, but not donor

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

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

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

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

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

154 to the development of both acute and chronic cardiac allograft rejection, and targeting donor selecti

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

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

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

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

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

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

161 after renal ischemia reperfusion injury and cardiac allograft rejection.

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

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

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

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

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

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

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

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

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

171 om naive B7-1/B7-2-/- mice readily initiated cardiac allograft rejection.

172 bute to viral and autoimmune myocarditis and cardiac allograft rejection.

173 ibute to the pathogenesis of myocarditis and cardiac allograft rejection.

174 in autoimmune and infectious myocarditis and cardiac allograft rejection.

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

176 complement activation leading to accelerated cardiac allograft rejection.

177 Equitable allocation of cardiac allografts requires further investigation of the

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

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

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

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

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

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

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

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

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

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

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

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

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

191 -mismatched recipients, and permit prolonged cardiac allograft survival in fully MHC mismatched recip

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

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

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

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

196 Cardiac allograft survival was markedly prolonged in the

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

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

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

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

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

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

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

204 cell surface interaction, therefore inducing cardiac allograft tolerance.

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

206 Riboflavin administered in the setting of cardiac allograft transplantation appears to be a powerf

207 required for tolerance in vivo, we performed cardiac allograft transplantation under conditions of co

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

209 in allograft rejection in a murine model of cardiac allograft transplantation.

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

211 factor 1 (AIF-1) was first identified in rat cardiac allografts undergoing chronic rejection.

212 Indeed, cardiac allografts underwent fulminant rejection in sens

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

214 rphonuclear leukocytes, acute rejection, and cardiac allograft vascular disease (CAV) assessed by int

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

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

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

218 Cardiac allograft vasculopathy (CAV) has a high prevalen

219 Cardiac allograft vasculopathy (CAV) has an incidence of

220 sessed clinical predictors of the process of cardiac allograft vasculopathy (CAV) in 39 consecutive p

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

222 eful model that has evolved for the study of cardiac allograft vasculopathy (CAV) is a heterotopic (a

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

224 Cardiac allograft vasculopathy (CAV) is a major limitati

225 Chronic rejection in transplanted hearts or cardiac allograft vasculopathy (CAV) is the leading caus

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

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

228 Cardiac allograft vasculopathy (CAV) is the preeminent c

229 Cardiac allograft vasculopathy (CAV) is the principal ca

230 Although cardiac allograft vasculopathy (CAV) is typically charac

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

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

233 Cardiac allograft vasculopathy (CAV) remains a leading c

234 Cardiac allograft vasculopathy (CAV) remains the Achille

235 Cardiac allograft vasculopathy (CAV) remains the leading

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

237 Cardiac allograft vasculopathy (CAV) was graduated in ac

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

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

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

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

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

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

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

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

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

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

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

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

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

251 4C T cells caused cardiac allograft vasculopathy in the absence of other T

252 Cardiac allograft vasculopathy is a key prognostic deter

253 Cardiac allograft vasculopathy is a major challenge to l

254 Cardiac allograft vasculopathy is a multifactorial proce

255 Cardiac allograft vasculopathy is the major cause of lat

256 Cardiac allograft vasculopathy is the major limiting fac

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

258 Cardiac allograft vasculopathy lesions contain alloreact

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

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

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

262 SRL as primary immunosuppression attenuates cardiac allograft vasculopathy progression.

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

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

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

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

267 tter understanding of the pathophysiology of cardiac allograft vasculopathy to direct interventions f

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

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

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

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

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

273 antation and reflects diastolic dysfunction, cardiac allograft vasculopathy, and poor late outcome.

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

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

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

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

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

279 Cardiac allograft vasculopathy, the nature of the inflam

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

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

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

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

284 well as to suppress the late development of cardiac allograft vasculopathy.

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

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

287 pharmacotherapies to halt the progression of cardiac allograft vasculopathy.

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

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

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

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

292 As expected, all cardiac allografts were acutely rejected.

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

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

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

296 Fully mismatched cardiac allografts were transplanted into alemtuzumab tr

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

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

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