ライフサイエンスコーパス: lung allograft

1 iver may bestow immunologic privilege to the lung allograft.

2 utcome can be achieved for an ABO-mismatched lung allograft.

3 of actively replicating CMV in the blood and lung allograft.

4 presence of TGF-beta1 in PBECs derived from lung allograft.

5 velopment of functional abnormalities of the lung allograft.

6 is and reduces late CMV infection within the lung allograft.

7 ytomegalovirus (CMV) reactivation within the lung allograft.

8 sponse and improves clearance of HA from the lung allograft.

9 chiolitis obliterans syndrome (BOS) in human lung allografts.

10 al proinflammatory cytokines/chemokines from lung allografts.

11 ) to Wistar-Kyoto (WKY) and PVG.R8 to PVG.1U lung allografts.

12 appearance, and reduced collagen content in lung allografts.

13 major histocompatibility complex mismatched lung allografts.

14 to investigate whether MAC causes injury to lung allografts.

15 recent study found minimal numbers of DC in lung allografts.

16 ncipal cause of acute and chronic failure of lung allografts.

17 tory pathway blockade may be useful in human lung allografts.

18 mRNA transcription in the BAL fluid of human lung allografts.

19 s obliterans could not be confirmed in human lung allografts.

20 kin graft survival in animals tolerized with lung allografts.

21 antation with donor-specific and third-party lung allografts.

22 donor-specific transplantation tolerance to lung allografts.

23 at, would confer donor-specific tolerance to lung allografts.

24 ls with rejection and/or infection of single lung allografts.

25 ial cells with rejection and/or infection of lung allografts.

26 al contractions is reduced with rejection of lung allografts.

27 operated dogs and dogs with rejecting single lung allografts.

28 l proliferation seen in chronic rejection of lung allografts.

29 at contributes to progression of fibrosis in lung allografts.

30 d for trafficking of these memory T cells to lung allografts.

31 ical role for CD8+ central memory T cells in lung allograft acceptance and highlight the need for tai

32 Therefore, new strategies to promote lung allograft acceptance are urgently needed.

33 e found that costimulatory blockade-mediated lung allograft acceptance depended on the rapid infiltra

34 Mechanistically, animals with lung allograft acceptance had established higher levels

35 we show that following the establishment of lung allograft acceptance in mice, Pseudomonas aeruginos

36 olleagues demonstrate in a murine model that lung allograft acceptance requires infiltration of a spe

37 eloablative conditioning regimen had durable lung allograft acceptance.

38 a paucity of data regarding the viability of lung allografts after a period of cardiac arrest in the

39 to bronchoalveolar secretions may injure the lung allograft and impair bacterial clearance, we assess

40 d mesenchymal stem cells is present in human lung allografts and can be isolated and expanded ex vivo

41 ing IL-17 recovered CRP expression in murine lung allografts and decreased local C3a production.

42 e to differentiate into Th17 cells, rejected lung allografts and developed OB similar to control mice

43 hanistic insight into the acute rejection of lung allografts and highlight the importance of identify

44 oproteinase (TIMP)-1 expression increases in lung allografts and is associated with the onset of allo

45 reactive T cells are initially primed within lung allografts and not in secondary lymphoid organs fol

46 rats develop a spontaneous tolerance to WKY lung allografts and show long-term retention of donor-sp

47 monstrate that MAC causes vascular injury in lung allografts and that the location of injury is depen

48 ssing costimulatory molecules are present in lung allografts, and costimulatory pathway blockade may

49 sing rejection and facilitating tolerance of lung allografts, and such discoveries are being validate

50 and/or enhance the immunological response to lung allograft antigens.

51 (pathologic grade A2 or A3) in recipients of lung allografts are a major risk factor for the subseque

52 Lung allografts are associated with high rates of reject

53 Lung allografts are prone to rejection, even though reci

54 Lung allografts are prone to reperfusion injury and acut

55 ry tract secretions of CF patients receiving lung allografts are sufficient in the majority of patien

56 nly provides new insights into the nature of lung allografts as a primary site where T and B cell pri

57 onstrate here that NK cells infiltrate mouse lung allografts before T cells and thereby diminished al

58 esenchymal cells (MCs) derived from fibrotic lung allografts (BOS MCs) demonstrated constitutive nucl

59 effective at preventing chronic rejection of lung allografts (bronchiolitis obliterans syndrome [BOS]

60 In animal models of acute rejection in lung allografts, bronchus-associated lymphoid tissue (BA

61 imited results with DCD pancreas, liver, and lung allografts (but not heart) are now approaching that

62 We conclude that de novo colonization of the lung allograft by Pseudomonas is strongly associated wit

63 hough CD8(+) T cells existed in the IDO-high lung allografts, CD8(+) T cells remained viable and coul

64 rane vesicles released from cells within the lung allograft, contain a diverse array of biomolecules

65 Here, we showed that tolerant lung allografts could induce and maintain tolerance of h

66 Here, studies of cells derived from human lung allografts demonstrate the presence of a multipoten

67 The revascularized lung allograft demonstrated a network of arterioles, cap

68 Rat lung allografts demonstrated a marked time-dependent inc

69 We demonstrate that human lung allograft-derived MSCs uniquely express embryonic l

70 dulator of fibrotic differentiation of human lung allograft-derived MSCs.

71 Up to 50% of human lung allografts develop chronic rejection manifested as

72 One third of human lung allografts develop chronic rejection manifested as

73 vide a unique opportunity to interrogate the lung allograft during BOS development and identify poten

74 quality of CMV-specific CD4(+) memory in the lung allograft during chronic infection, and show an imp

75 LT3, were isolated from F344 (RT1(lv1)) rat lung allografts during rejection that occurred after tra

76 Baseline lung allograft dysfunction (BLAD) is characterized by th

77 correlate with an increased risk of chronic lung allograft dysfunction (CLAD) and a poorer survival.

78 riage would not increase the risk of chronic lung allograft dysfunction (CLAD) and graft loss, severe

79 Chronic lung allograft dysfunction (CLAD) and its obstructive fo

80 y, would lead to the highest risk of chronic lung allograft dysfunction (CLAD) and that a type I immu

81 ng transplantation, both frailty and chronic lung allograft dysfunction (CLAD) commonly develop, and

82 A-G (HLA-G EV ) levels could predict chronic lung allograft dysfunction (CLAD) development.

83 suggests a restrictive phenotype of chronic lung allograft dysfunction (CLAD) exists; however, the o

84 ired respiratory viruses (CARVs) and chronic lung allograft dysfunction (CLAD) in lung transplant rec

85 Chronic lung allograft dysfunction (CLAD) is a major cause of al

86 Chronic lung allograft dysfunction (CLAD) is the leading cause o

87 Chronic lung allograft dysfunction (CLAD) is the main reason for

88 Chronic lung allograft dysfunction (CLAD) is the major barrier t

89 Chronic lung allograft dysfunction (CLAD) is the major factor li

90 Chronic lung allograft dysfunction (CLAD) is the major limitatio

91 Chronic lung allograft dysfunction (CLAD) is the major outcome l

92 Chronic lung allograft dysfunction (CLAD) is the most common cau

93 before transplant on development of Chronic Lung Allograft Dysfunction (CLAD) or CLAD-related death.

94 gnificant difference in freedom from chronic lung allograft dysfunction (CLAD) or survival between th

95 Chronic lung allograft dysfunction (CLAD) phenotype determines p

96 Chronic lung allograft dysfunction (CLAD) remains a major cause

97 Chronic lung allograft dysfunction (CLAD) remains a major hurdle

98 Chronic lung allograft dysfunction (CLAD) remains one of the maj

99 ferential diagnosis of phenotypes of chronic lung allograft dysfunction (CLAD) remains troublesome.

100 Chronic lung allograft dysfunction (CLAD), and especially bronch

101 Chronic lung allograft dysfunction (CLAD), presenting as bronchi

102 Background Chronic lung allograft dysfunction (CLAD), the physiologic corre

103 s of dnDSA with patient survival and chronic lung allograft dysfunction (CLAD), were determined using

104 (CMV) infection is a risk factor for chronic lung allograft dysfunction (CLAD), which limits survival

105 bronchoalveolar lavage (BAL) fluid, chronic lung allograft dysfunction (CLAD)-free survival and over

106 Chronic lung allograft dysfunction (CLAD)-free survival was also

107 mainly limited by the development of chronic lung allograft dysfunction (CLAD).

108 Early lung allograft dysfunction (ischemia-reperfusion injury)

109 Subjects with severe chronic lung allograft dysfunction (n = 13) reported significant

110 tly worse HRQL than subjects without chronic lung allograft dysfunction (n = 168) on 6 of the 10 LT-Q

111 ucing the incidence of severe AR and chronic lung allograft dysfunction and improving outcomes.

112 transplantation, is associated with chronic lung allograft dysfunction and worse post-transplantatio

113 We hypothesize that patients with chronic lung allograft dysfunction can be subdivided by exercise

114 blood viremia, acute rejection, and chronic lung allograft dysfunction did not differ between the 2

115 anisms leading to the development of chronic lung allograft dysfunction following de novo development

116 ar rejection is a key contributor to chronic lung allograft dysfunction following transplantation; wh

117 Chronic lung allograft dysfunction is a heterogeneous entity lim

118 Chronic lung allograft dysfunction is a multifactorial disease t

119 Advanced chronic lung allograft dysfunction limits survival after lung tr

120 Chronic lung allograft dysfunction manifests as bronchiolitis ob

121 nferred a 2.2-fold increased risk of chronic lung allograft dysfunction or death (time-dependent P <

122 Heterogeneity of patients with advanced lung allograft dysfunction regarding exercise tolerance

123 her with those of others that relate chronic lung allograft dysfunction to an increase in BALF neutro

124 g-term management remains limited by chronic lung allograft dysfunction, an umbrella term used for a

125 ses (CARV) can accelerate the development of lung allograft dysfunction, but the immunologic mechanis

126 bliterans syndrome, a common form of chronic lung allograft dysfunction, is the major limitation to l

127 Moreover, chronic lung allograft dysfunction-free (P = 0.86) and overall s

128 core within 72 hours) and long-term (chronic lung allograft dysfunction-free and overall survival) fo

129 dysfunction after AMR and decreased chronic lung allograft dysfunction-free survival.

130 erial circulation appears to trigger chronic lung allograft dysfunction.

131 XCR3 chemokines as biomarkers for subsequent lung allograft dysfunction.

132 d use at 1 year and time to onset of chronic lung allograft dysfunction.

133 lial cell IL-12 family members could mediate lung allograft dysfunction.

134 ans syndrome is the leading cause of chronic lung allograft dysfunction.

135 use at 1 year, and time to onset of chronic lung allograft dysfunction.

136 ransplantation is the development of chronic lung allograft dysfunction.

137 rmine whether T cells infiltrating rejecting lung allografts employed restricted V beta elements.

138 o create a state of operational tolerance to lung allografts even in the presence of donor-sensitized

139 he presence of MSCs of donor sex identity in lung allografts even years after transplantation provide

140 RATIONALE: The predominant cause of chronic lung allograft failure is small airway obstruction arisi

141 ellular immunity is the reputed mechanism of lung allograft failure.

142 aps (NETs) have been implicated in liver and lung allograft failures.

143 on-Fib MCs), MCs derived from fibrotic human lung allografts (Fib-MCs) demonstrated increased phospho

144 The availability of suitable lung and heart-lung allografts for transplantation remains poor.

145 ic pulmonary fibrosis received a left single-lung allograft from a blood type A donor.

146 Lung allografts from beta-catenin reporter mice demonstr

147 control animals, the swine transplanted with lung allografts from brain dead donors all rejected thei

148 In contrast, lung allografts from C6-deficient (C6(-)) donors to C6(-

149 Lung and heart-lung allografts from HBcAb positive donors may be safely

150 Adult recipients of lung allografts from these arrest/resuscitation donors b

151 Rat lung allografts fully incompatible at MHC class I and II

152 ress the exact roles of lymphatic vessels in lung allograft function and survival are limited.

153 was performed to evaluate rehospitalization, lung allograft function, and secondary infections up to

154 ests that ECP can slow the loss or stabilize lung allograft function, treatment is often initiated on

155 ols had similar baseline characteristics and lung allograft function.

156 sence of CXCL9 and CXCL10 portents worsening lung allograft function; measuring these IFNG-induced ch

157 Control lung allografts (group 2) survived on average 45 days (r

158 The lung allografts had histologic features resembling human

159 c(+) dendritic cells (DCs) within orthotopic lung allografts immediately after reperfusion.

160 Rejection of lung allografts in group 1 occurred at a median of 6.5 d

161 tion within the microvessels of transplanted lung allografts in nude mice.

162 tical role of Foxp3+ T cells residing within lung allografts in the regulation of AMR.

163 Pre-existing lung allograft injury from donor-directed Abs or gastroe

164 pirfenidone, an anti-fibrotic agent, reduces lung allograft injury or rejection.

165 results demonstrate that IDO prevents acute lung allograft injury through augmenting the local antio

166 up-regulation of IDO could ameliorate acute lung allograft injury.

167 studies demonstrate that the revascularized lung allograft is responsive to various external stimuli

168 The chronic rejection of lung allografts is attributable to progressive small air

169 lung transplantation that acute rejection of lung allografts is independent of CD4(+) T cell-mediated

170 e role of CD4(+) T cells in the rejection of lung allografts is largely unknown.

171 prevent rejection of fully MHC incompatible lung allografts is unknown.

172 We conclude that studies of lung allografts may underestimate DC numbers if relying

173 ppressive efficacy in a highly stringent rat lung allograft model.

174 Examination of lung allograft mononuclear cells obtained by bronchoalve

175 ve immunosuppression, acute rejection of the lung allograft occurs in over half of transplant recipie

176 By depleting Brown Norway (BN, RT1n) rat lung allografts of AM before transplantation into Lewis

177 resence of unopposed NE activity in BAL from lung allografts of patients with CF is associated with p

178 s among CD4 cells in BAL may help to predict lung allograft outcome and guide therapeutic immunosuppr

179 he risks of virus transmission and long-term lung allograft outcomes are not as well described when u

180 he specific role of complement activation in lung allograft pathology, IL-17 production, and OB is un

181 SH in bronchoalveolar lavage fluid (BALF) in lung allograft patients in the absence and presence of a

182 SP-D fragments are present in the BAL of CF lung allograft patients.

183 of spirometry to assess the function of the lung allograft post-transplant, we retrospectively revie

184 Furthermore, DC-depleted lung allografts presented decreased signs of rejection.

185 re overexpressed by gene therapy in F344 rat lung allografts prior to transplantation into WKY recipi

186 uces long-term tolerance to fully mismatched lung allografts procured from healthy MHC-inbred miniatu

187 In lung allografts, progressive terminal airway fibrosis le

188 PFD has lung allograft protective properties, and in addition to

189 The experimental rat lung allograft proved attractive for evaluating effector

190 Successful management of an ABO-mismatched lung allograft recipient has not previously been describ

191 ry muscle function in nine clinically stable lung allograft recipients (six men and three women, aged

192 nt of obliterative bronchiolitis among human lung allograft recipients and provides a novel and easil

193 We conclude that stable lung allograft recipients experience expiratory and lowe

194 by means of polymerase chain reaction in 93 lung allograft recipients for functional polymorphisms i

195 el that mimics obliterative bronchiolitis of lung allograft recipients in human airways in vivo.

196 TES involvement in lung allograft rejection, lung allograft recipients were passively immunized with

197 Actuarial survival of lung allograft recipients with anti-HLA antibodies (n =

198 otopheresis (ECP) and mortality after ECP in lung allograft recipients with bronchiolitis obliterans.

199 In previous studies of cynomolgus monkey lung allograft recipients, we demonstrated significant i

200 dysfunction (CLAD), which limits survival in lung allograft recipients.

201 vage (BAL) of five healthy volunteers and 27 lung allograft recipients.

202 identified on transbronchial biopsy in human lung allograft recipients.

203 olar lavage samples were obtained from human lung allograft recipients.

204 obliterative bronchiolitis in heart-lung and lung allograft recipients.

205 to currently available methods of monitoring lung allograft recipients.

206 a-chain variable gene (TCRBV) repertoires in lung allograft recipients.

207 et the challenges of a growing population of lung allograft recipients.

208 ity should be clinically explored to prepare lung allograft recipients.

209 orking formulation for the classification of lung allograft rejection (), and devised a quantitative

210 n in a highly histoincompatible model of rat lung allograft rejection (AR).

211 fic CD8+ CTLs in the pathogenesis of chronic lung allograft rejection (bronchiolitis obliterans syndr

212 ry allograft function and diagnosing chronic lung allograft rejection after lung transplantation (LTx

213 vo neutralization of RANTES attenuated acute lung allograft rejection and reduced allospecific respon

214 The incidence and the severity of acute lung allograft rejection has been linked to the developm

215 However, the effect of MMP inhibition on lung allograft rejection has not been reported.

216 investigated RANTES involvement during acute lung allograft rejection in humans and in a rat model sy

217 mportant role in the pathogenesis of chronic lung allograft rejection in humans.

218 immunogenic self-protein, can induce chronic lung allograft rejection in rodent models.

219 8/B7 costimulatory pathways attenuates acute lung allograft rejection in the absence of CD4(+) T cell

220 Chronic lung allograft rejection in the form of bronchiolitis ob

221 We have reported that lung allograft rejection involves an immune response to

222 Collectively, these data show that lung allograft rejection involves both allo- and autoimm

223 Chronic lung allograft rejection is associated with a progressiv

224 Acute lung allograft rejection is believed to be initiated by

225 Rat lung allograft rejection is mediated by collagen type V

226 The histology and immunology of lung allograft rejection is postulated to result from do

227 Chronic lung allograft rejection is the single most important ca

228 ases (MMPs) has been associated with chronic lung allograft rejection known as bronchiolitis oblitera

229 xperimental models of ulcerative colitis and lung allograft rejection led us to test the effect of th

230 xpression of CXCR3, resulting in lower acute lung allograft rejection scores.

231 Chronic lung allograft rejection was associated with the loss of

232 Our algorithm predicts heart and lung allograft rejection with an accuracy that is simila

233 MMPs and TIMPs in the immunopathogenesis of lung allograft rejection, and indicate their effects are

234 llectively, these data illustrate that human lung allograft rejection, but not pulmonary infection, i

235 Chronic lung allograft rejection, known as obliterative bronchio

236 To determine RANTES involvement in lung allograft rejection, lung allograft recipients were

237 Chronic human lung allograft rejection, represented by bronchiolitis o

238 is increasingly recognized to contribute to lung allograft rejection, the significance of endogenous

239 tify patients with increased risk of chronic lung allograft rejection, we assessed the utility of an

240 to what extent NK cells can influence mouse lung allograft rejection.

241 nsidered to reflect the evolution of chronic lung allograft rejection.

242 me, the predominant manifestation of chronic lung allograft rejection.

243 potentially clinically relevant mechanism of lung allograft rejection.

244 collagen (col(V)) is a major risk factor for lung allograft rejection.

245 is the histopathological finding in chronic lung allograft rejection.

246 ithelium is considered as a major target for lung allograft rejection.

247 t into the immune mechanisms responsible for lung allograft rejection.

248 sociated with alloimmunity and chronic human lung allograft rejection.

249 une mediated response is involved in chronic lung allograft rejection.

250 future clinical studies in the prevention of lung allograft rejection.

251 with a mutant TLR4 genotype manifest reduced lung allograft rejection.

252 tment of mononuclear cells, leading to acute lung allograft rejection.

253 a pivotal event in the pathogenesis of acute lung allograft rejection.

254 fluid have been associated with human acute lung allograft rejection.

255 me, which is considered to represent chronic lung allograft rejection.

256 important role in the pathogenesis of acute lung allograft rejection.

257 nduced the histology and immunology of acute lung allograft rejection.

258 ne the role of ICAM-1 on donor lung cells in lung allograft rejection.

259 cts on the histology and immunology of acute lung allograft rejection.

260 ide synthase (iNOS) ameliorated severe acute lung allograft rejection.

261 amma and IgG subtypes, locally, during acute lung allograft rejection.

262 tive Treg were insufficient to prevent acute lung allograft rejection.

263 hange microRNAs (miRNAs), leading to chronic lung allograft rejection.

264 further deaths from pulmonary infection and lung allograft rejection.

265 AM-1 are all important adhesion molecules in lung allograft reperfusion injury--yet even with antibod

266 , Mac-1, and ICAM-1 in a rat model of severe lung allograft reperfusion injury.

267 IDO overexpression in lung allografts resulted in a significant protective eff

268 is caused by a fibroproliferative process in lung allografts resulting in irreversible damage.

269 ropositive) who received a HLA-B27 bilateral lung allograft showed a dynamic expansion of the cross-r

270 GE2 treatment of LR-MSCs derived from normal lung allografts significantly inhibited their proliferat

271 nce that lymphatic vessel formation improves lung allograft survival in a murine transplant model.

272 , we conducted a comprehensive assessment of lung allograft survival in this population.

273 passenger leukocytes significantly prolongs lung allograft survival.

274 multiple drivers of leukocyte recruitment in lung allografts that contribute to lymphocytic bronchiti

275 icantly increase the available pool of donor lung allografts through the reconditioning of "marginal"

276 dent on lymphatic drainage from the tolerant lung allograft to the periphery.

277 tal GSH in the alveolar fluid may predispose lung allografts to extracellular H2O2-mediated toxicity.

278 ophages may increase susceptibility of human lung allografts to the rejection process.

279 ta provide proof-of-concept for establishing lung allograft tolerance with tandem donor bone marrow t

280 recipients of single (100) or bilateral (52) lung allografts transplanted at our institution between

281 Lungs from patients with rejected lung allografts treated by a second transplant (n = 7) w

282 sults show that C57BL/6 recipients of BALB/c lung allografts undergoing this complete short-duration

283 munosuppression-mediated acceptance of mouse lung allografts unless G-CSF-mediated granulopoiesis is

284 t numbers and phenotype of macrophages/DC in lung allografts using endobronchial biopsy (EBB) and tra

285 wed that Foxp3+ cells egressed from tolerant lung allografts via lymphatics and were recruited into d

286 C6 production by lung allografts was demonstrated at the mRNA and protein

287 differentiation of MSCs isolated from normal lung allografts was noted in the presence of profibrotic

288 DC activation from lung allografts was suppressed with PFD, and there seeme

289 Moreover, both responses in the PBMC and lung allograft were found to persist, despite substantia

290 All donor-specific lung allografts were accepted by mixed chimeras (n = 40)

291 Lung allografts were performed from C6(-) donors to C6(+

292 d operative techniques, four orthotopic left lung allografts were performed using MHC-matched, minor-

293 Separately, WKY rats that received F344 lung allografts were treated systemically with COL-3, a

294 ologic features of hyperacute rejection in a lung allograft which are similar to those seen with othe

295 Seventy-six recipients of double lung allografts who underwent MR imaging of the lungs du

296 Stimulation of the lung allograft with TNF-alpha induced leukocyte rolling

297 Lung allografts with the SP-D polymorphic variant Thr(11

298 at was the incidence of CMV infection in the lung allograft within 18 months of LTx was significantly

299 iology, we hypothesized an orthotopic ferret lung allograft would develop OB.

300 that NKG2C NK cells responding to CMV in the lung allograft would reduce CMV-related inflammation and