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 sponse and improves clearance of HA from the lung allograft.

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

5 appearance, and reduced collagen content in lung allografts.

6 major histocompatibility complex mismatched lung allografts.

7 to investigate whether MAC causes injury to lung allografts.

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

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

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

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

12 kin graft survival in animals tolerized with lung allografts.

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

14 donor-specific transplantation tolerance to lung allografts.

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

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

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

18 al contractions is reduced with rejection of lung allografts.

19 operated dogs and dogs with rejecting single lung allografts.

20 l proliferation seen in chronic rejection of lung allografts.

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

22 at contributes to progression of fibrosis in lung allografts.

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

24 al proinflammatory cytokines/chemokines from lung allografts.

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

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

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

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

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

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

31 eloablative conditioning regimen had durable lung allograft acceptance.

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

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

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

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

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

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

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

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

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

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

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

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

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

45 Lung allografts are associated with high rates of reject

46 Lung allografts are prone to rejection, even though reci

47 Lung allografts are prone to reperfusion injury and acut

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

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

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

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

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

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

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

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

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

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

58 Rat lung allografts demonstrated a marked time-dependent inc

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

80 Early lung allograft dysfunction (ischemia-reperfusion injury)

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

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

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

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

85 Chronic lung allograft dysfunction is a heterogeneous entity lim

86 Chronic lung allograft dysfunction is a multifactorial disease t

87 Advanced chronic lung allograft dysfunction limits survival after lung tr

88 Chronic lung allograft dysfunction manifests as bronchiolitis ob

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

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

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

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

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

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

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

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

97 ransplantation is the development of chronic lung allograft dysfunction.

98 XCR3 chemokines as biomarkers for subsequent lung allograft dysfunction.

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

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

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

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

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

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

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

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

107 Lung allografts from beta-catenin reporter mice demonstr

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

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

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

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

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

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

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

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

116 The lung allografts had histologic features resembling human

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

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

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

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

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

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

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

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

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

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

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

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

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

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

131 Examination of lung allograft mononuclear cells obtained by bronchoalve

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

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

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

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

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

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

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

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

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

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

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

143 In lung allografts, progressive terminal airway fibrosis le

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

145 The experimental rat lung allograft proved attractive for evaluating effector

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

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

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

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

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

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

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

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

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

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

156 identified on transbronchial biopsy in human lung allograft recipients.

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

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

159 to currently available methods of monitoring lung allograft recipients.

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

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

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

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

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

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

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

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

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

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

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

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

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

173 8/B7 costimulatory pathways attenuates acute lung allograft rejection in the absence of CD4(+) T cell

174 Chronic lung allograft rejection in the form of bronchiolitis ob

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

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

177 Chronic lung allograft rejection is associated with a progressiv

178 Acute lung allograft rejection is believed to be initiated by

179 Rat lung allograft rejection is mediated by collagen type V

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

181 Chronic lung allograft rejection is the single most important ca

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

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

184 Chronic lung allograft rejection was associated with the loss of

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

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

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

188 Chronic lung allograft rejection, known as obliterative bronchio

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

190 Chronic human lung allograft rejection, represented by bronchiolitis o

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

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

193 potentially clinically relevant mechanism of lung allograft rejection.

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

195 is the histopathological finding in chronic lung allograft rejection.

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

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

198 sociated with alloimmunity and chronic human lung allograft rejection.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

224 passenger leukocytes significantly prolongs lung allograft survival.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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