ライフサイエンスコーパス: allograft rejection

1 efined roles in the pathophysiology of renal allograft rejection.

2 zation increases the risk of T cell-mediated allograft rejection.

3 as a potential prognosis marker for chronic allograft rejection.

4 es the loss of immune tolerance and promotes allograft rejection.

5 novo after lung transplantation and mediate allograft rejection.

6 Treg were insufficient to prevent acute lung allograft rejection.

7 osuppressants which are essential to prevent allograft rejection.

8 e T lymphocytes are the primary mediators of allograft rejection.

9 olid organ transplants, primarily because of allograft rejection.

10 ly, our study demonstrated that aging delays allograft rejection.

11 ched, life-sustaining, murine model of renal allograft rejection.

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

13 anti-programmed cell death-1 (PD-1)-related allograft rejection.

14 22 SNPs on the susceptibility to acute liver allograft rejection.

15 une responses that drive atherosclerosis and allograft rejection.

16 raft model, resulting in rapid acute cardiac allograft rejection.

17 and have been implicated in the mediation of allograft rejection.

18 mphoma, graft-versus-host disease, and organ allograft rejection.

19 tion of the alloantibody response, and rapid allograft rejection.

20 otoxic CD8 T-cell responses that cause rapid allograft rejection.

21 cells (ECs) damaged during transplant drives allograft rejection.

22 peutic target to reduce this form of corneal allograft rejection.

23 eases such as cancer, lymphedema, and tissue allograft rejection.

24 eyes developed typical clinical signs of an allograft rejection.

25 al in directing host immune reactions toward allograft rejection.

26 ications, bleedings, anastomotic leakage, or allograft rejection.

27 reduced side effects in patients with renal allograft rejection.

28 y have a protective role and attenuate overt allograft rejection.

29 phology were found to "announce" an upcoming allograft rejection.

30 reactivity including autoimmune diseases and allograft rejection.

31 Little data exist on these markers during allograft rejection.

32 pendently predicts a decreased risk of acute allograft rejection.

33 locks memory and attenuates kidney and heart allograft rejection.

34 tute promising approaches for the control of allograft rejection.

35 ffector T cells in situ, and correlated with allograft rejection.

36 n between isolation and transplantation, and allograft rejection.

37 latation and permeability is observed during allograft rejection.

38 play an important role in acute and chronic allograft rejection.

39 unopathology in human autoimmune disease and allograft rejection.

40 dy-producing plasma cells to reverse humoral allograft rejection.

41 T cell responses that drive autoimmunity and allograft rejection.

42 that underlies IL-4 neutralization-resistant allograft rejection.

43 rate with other effector mechanisms to cause allograft rejection.

44 mation, and that NK-cell deficiency enhanced allograft rejection.

45 hat extent NK cells can influence mouse lung allograft rejection.

46 yte globulin (ATG) have been shown to reduce allograft rejection.

47 is reported to promote KS regression without allograft rejection.

48 llular and humoral mechanisms of acute renal allograft rejection.

49 fic activated (Bonzo) T cells during corneal allograft rejection.

50 nt activation leading to accelerated cardiac allograft rejection.

51 plantation model was used for studying acute allograft rejection.

52 -fms kinase inhibitor (fms-I) in acute renal allograft rejection.

53 r the amelioration of human autoimmunity and allograft rejection.

54 gets in some liver diseases, including acute allograft rejection.

55 in animal models of autoimmune disorders and allograft rejection.

56 wly generated host Tregs can prevent chronic allograft rejection.

57 nologic mechanism underlying smoking-related allograft rejection.

58 ssion of Bcl-xL in Drak2-/- T cells restored allograft rejection.

59 h revokes immune privilege, prevents corneal allograft rejection.

60 terize the metabolomic profile of intestinal allograft rejection.

61 red to reflect the evolution of chronic lung allograft rejection.

62 he predominant manifestation of chronic lung allograft rejection.

63 but its clinical applicability is limited by allograft rejection.

64 eficiency prevented T-cell priming and islet allograft rejection.

65 SF25 agonists expand Tregs in vivo and delay allograft rejection.

66 ST), although it failed to alter acute islet allograft rejection.

67 ched, life-sustaining murine model of kidney allograft rejection.

68 s also play a role in bone marrow cell (BMC) allograft rejection.

69 city and endothelial vasculopathy in chronic allograft rejection.

70 ehavior; values >=2.5 are predictive of late allograft rejection.

71 transplanted graft and potentiate subsequent allograft rejection.

72 suggest therapeutic approaches to ameliorate allograft rejection.

73 splant and was independently associated with allograft rejection.

74 nnate immune system plays a critical role in allograft rejection.

75 on strategies have led to a decline in acute allograft rejection.

76 molecular analysis in the diagnosis of renal allograft rejection.

77 as a potential therapeutic target to control allograft rejection.

78 her deaths from pulmonary infection and lung allograft rejection.

79 onin 1-deficient T cells actively suppressed allograft rejection.

80 hy, ureteral obstructive disease, and kidney allograft rejection.

81 in CD4(+) T effectors fails to inhibit acute allograft rejection.

82 s of immunological memory that contribute to allograft rejection.

83 ation to identify antibodies associated with allograft rejection.

84 cularly among patients with CMV infection or allograft rejection.

85 ing variants may represent a risk factor for allograft rejection.

86 lure, and the immunological basis of corneal allograft rejection.

87 bodies of the IgE isotype are induced during allograft rejection.

88 wo-stage genetic association study of kidney allograft rejection.

89 robial pathogens but is also responsible for allograft rejection.

90 ears, we did not detect any signs of corneal allograft rejection.

91 ective cure of HCV infection without risk of allograft rejection.

92 e for an important role of IL-6 in mediating allograft rejection.

93 stablish the role of RIP3 in chronic cardiac allograft rejection.

94 on and T cell priming, ultimately leading to allograft rejection.

95 s of kidney dysfunction and acute or chronic allograft rejection.

96 sM(C)(re) Mtor(fl/fl) ) did not affect acute allograft rejection.

97 ell numbers in naive mice and hastened islet allograft rejection.

98 o the response to steroid treatment of acute allograft rejection.

99 s (0.2%), respectively, and 7 eyes developed allograft rejection (0.7%).

100 a (29.3% vs. 11.6%, respectively; P < .001), allograft rejection (16.6% vs. 1.7%, respectively; P < .

101 After 6 months, the main complications were allograft rejection (2.4%) and secondary graft failure (

102 The incidence of allograft rejection (28% vs 25%; difference, 3% [95% CI,

103 th anti-VA dnDSAs had a higher rate of organ allograft rejection (45.4% vs 13.8%, P = .03) compared t

104 hways involved in immune responses including allograft rejection (6.69) and graft-versus-host disease

105 sidered a new option to inhibit the onset of allograft rejection acting on BOS specific features.

106 of blood and lymphatic neovessels and rapid allograft rejection after corneal penetrating keratoplas

107 Such strategies tend to detect allograft rejection after significant injury has already

108 as multiple sclerosis, rheumatoid arthritis, allograft rejection after transplantation, and also in c

109 hich is implicated in the process of chronic allograft rejection, also known as transplant vasculopat

110 tively deplete monocyte/macrophages in acute allograft rejection, although this did not result in sig

111 development of future strategies to prevent allograft rejection.Although both direct and indirect pa

112 Subclinical antibody-mediated allograft rejection (AMR) has been characterized in seri

113 overy resulted in markedly accelerated heart allograft rejection and augmented host effector antibody

114 serve as sentinels for early recognition of allograft rejection and be targets for future therapies.

115 inting efficacy in the prevention of chronic allograft rejection and carry unacceptable risks includi

116 inhibiting IL-6/IL-6R to ameliorate chronic allograft rejection and coronary allograft vasculopathy.

117 risks associated with incidences of chronic allograft rejection and decreased survival in transplant

118 ) mouse model of T-cell-mediated human islet allograft rejection and developed a therapeutic regimen

119 mportant risk factor for accelerated cardiac allograft rejection and graft dysfunction .

120 obulins (ATGs) are used to prevent and treat allograft rejection and graft versus host disease.

121 currently being tested in trials to control allograft rejection and graft versus host disease.Thymic

122 T cells (Tregs) is a promising treatment for allograft rejection and graft-versus-host disease (GVHD)

123 ate goal of utilising Tregs as treatment for allograft rejection and graft-versus-host disease (GvHD)

124 ntitative technique for serial monitoring of allograft rejection and has potential application in hum

125 profiling in the setting of diagnosing renal allograft rejection and how this will improve transplant

126 h protected them from both acute and chronic allograft rejection and increased their survival after t

127 quent, quantitative, and safer assessment of allograft rejection and injury status.

128 Thus, dd-cfDNA may be used to assess allograft rejection and injury; dd-cfDNA levels <1% refl

129 Allograft rejection and late endothelial failure account

130 Irreversible allograft rejection and late endothelial failure account

131 quences would provide essential insight into allograft rejection and lead to better therapies for tra

132 , where infections have been associated with allograft rejection and may be a causal event precipitat

133 nnate immune signaling pathways that promote allograft rejection and neutrophilia.

134 ecipients is limited because of the risk for allograft rejection and poor tolerability.

135 ecipients is limited because of the risk for allograft rejection and poor tolerability.

136 key role in transplantation by accelerating allograft rejection and preventing tolerance induction.

137 ific and effective therapy for prevention of allograft rejection and prolongation of graft survival.

138 mbers ex vivo and have been shown to prevent allograft rejection and promote tolerance in animal mode

139 ent regulatory axis in T cells important for allograft rejection and suggest that modulation of this

140 s in the phenotype of BEC during acute liver allograft rejection and the mechanism driving these chan

141 aim to define the role of P2XRs during islet allograft rejection and to establish a novel anti-P2XRs

142 shown to be a promising approach to prevent allograft rejection and to treat autoimmune and inflamma

143 determine the function of IL-6 in regulating allograft rejection and tolerance, BALB/c cardiac grafts

144 To shed light on the dynamics of ITx allograft rejection and treatment resistance, peripheral

145 atory responses in the allograft, leading to allograft rejection and vasculopathy.

146 emonstrate signatures of 'PD-1 signalling', 'allograft rejection' and 'T-cell receptor signalling', a

147 port preclinical studies of human pathogens, allograft rejection, and human T-cell function.

148 included 1-year survival, cardiac or hepatic allograft rejection, and infection.

149 ment of autoimmune disease and prevention of allograft rejection, and our findings help inform therap

150 variables: cytomegalovirus (CMV) infection, allograft rejection, and prophylaxis.

151 t macrophages are essential in acute cardiac allograft rejection, and selective depletion of macropha

152 cal role in the development of autoimmunity, allograft rejection, and spontaneous as well as therapy-

153 eligibility, organ selection, prophylaxis of allograft rejection, and supportive care would assist he

154 M2 cells is critical for preventing chronic allograft rejection, and that graft survival under such

155 ed a role for the purinergic system in islet allograft rejection, and the targeting of P2X7R is a nov

156 95% confidence interval {CI}, 2.0-10.5]) and allograft rejection (aOR, 3.0 [95% CI, 1.5-6.1]) signifi

157 al biomarker assays for future occurrence of allograft rejection (AR) are scarce.

158 ted, patients experience high rates of acute allograft rejection (AR).

159 l of understanding how immune adaptation and allograft rejection are linked, and conversely how a sys

160 required for in vivo-mismatched bone marrow allograft rejection as well as for NK memory responses t

161 e evidence regarding antibody-mediated liver allograft rejection at the 11th, 12th, and 13th meetings

162 nts, we found a significant association with allograft rejection at the LIMS1 locus represented by rs

163 o evaluate the contribution of mast cells to allograft rejection at the ocular surface.

164 e have been implicated as effectors in acute allograft rejection based on short-term depletion studie

165 ivation of genes related to inflammation and allograft rejection but downregulation of oxidative phos

166 transplant recipients is crucial to prevent allograft rejection, but increases risk for infectious d

167 on and adaptive immunity under conditions of allograft rejection, but little is known regarding their

168 phages are recognized as a hallmark of acute allograft rejection, but the roles that they play are no

169 igate the role of macrophages in acute heart allograft rejection by cellular and functional MRI with

170 cin has the potential to inhibit human islet allograft rejection by expanding CD4(+)FOXP3(+) Tregs in

171 ecific mechanisms involved in suppression of allograft rejection by helminth parasites could lead tow

172 act as antigen-presenting cells to initiate allograft rejection by host memory T cells.

173 in murine models of acute or chronic cardiac allograft rejection by transplanting recipients that eit

174 Heat shock protein-27 delays allograft rejection, by inhibiting tissue damage, throug

175 Kidney allograft rejection can occur in clinically stable patie

176 (CsA), an immunosuppressant used to prevent allograft rejection, can also increase the risk of RCC i

177 expressing Th2 cells, which promptly induced allograft rejection characterized by a Th2-type intragra

178 spects for defining a vascularized composite allograft rejection classification.

179 Allograft rejection continues to be a vexing problem in

180 f bm12 allografts led to accelerated cardiac allograft rejection, despite similar mean BP and serum s

181 Potent immunosuppression to prevent allograft rejection does not fully inhibit the productio

182 The primary endpoint of the study was acute allograft rejection during a 1-year follow-up period.

183 t functions in cancer immunosurveillance, BM allograft rejection, fighting infections, tissue homeost

184 ally by us and others as a means of reducing allograft rejection following organ transplantation.

185 ate a rejection episode and/or to prevent an allograft rejection from clinically manifesting itself.

186 tive cut-off, accurately discriminates acute allograft rejection from other causes of AKI in follow-u

187 osis of AKI, accurately discriminating acute allograft rejection from other causes of AKI in renal al

188 tely and rapidly differentiate patients with allograft rejection from patients with stable organ func

189 This Genomics of Chronic Allograft Rejection (GoCAR) study is a prospective, mult

190 nts from the prospective Genomics of Chronic Allograft Rejection (GoCAR) study who underwent surveill

191 to estimate the time-related probability of allograft rejection, graft failure, and KC recurrence.

192 sed to prevent or treat organ or bone-marrow allograft rejection, graft versus host disease, and auto

193 ly confirmed and clinically relevant chronic allograft rejection (group 2); 16 of these have already

194 Corneal allograft rejection has been described as a Th1-mediated

195 The role of NK cells in kidney allograft rejection has not been studied.

196 The changing epidemiology of cardiac allograft rejection has prompted many to question the yi

197 A antiendothelial cell antibodies (AECAs) in allograft rejection; however, evidence linking AECAs of

198 ory populations have the capacity to inhibit allograft rejection; however, their compensatory capacit

199 that, whereas Th17 cells predictably promote allograft rejection, IL-4-producing GATA-3(+) Th2 cells,

200 nsplantation, NKRs have been shown to assist allograft rejection in a CD28-independent fashion.

201 vo expanded human T(reg) to inhibit vascular allograft rejection in a humanized mouse model of arteri

202 e that blockade of IL-21 signaling can delay allograft rejection in a humanized skin transplantation

203 21R) blocking antibody on the early phase of allograft rejection in a humanized skin transplantation

204 Moreover, exacerbation of corneal allograft rejection in allergic mice was reversed by adm

205 Corneal allograft rejection in BALB/c allergic hosts was analyze

206 IgG alloantibodies that contribute to heart allograft rejection in CD40-/- heart recipients.

207 t depletion of CD8(+) cells that resulted in allograft rejection in half of the recipients.

208 Moreover, cardiac allograft rejection in HFD mice was modestly accelerated

209 ansgenic expression of Bcl-xL restored islet allograft rejection in IkappaBalphaDeltaN-Tg mice.

210 ntibodies and autoantibodies are involved in allograft rejection in kidney and heart transplantation.

211 in type A receptor (ETAR) is associated with allograft rejection in kidney and heart transplantation.

212 of new LVs has been shown to trigger chronic allograft rejection in kidney transplants.

213 mental autoimmune encephalomyelitis or islet allograft rejection in murine models.

214 CD4 TFH/GC B cell numbers and hastened islet allograft rejection in naive 12-week old Qa-1 deficient

215 154 pathway has been effective at preventing allograft rejection in numerous transplantation models.

216 e at constraining B cell responses and heart allograft rejection in sensitized recipients.

217 SAs) have all been implicated in accelerated allograft rejection in sensitized recipients.

218 Moreover, Eomes may rescue Th1-mediated allograft rejection in the absence of IL-4, T-bet, and R

219 therapy that provides protection from early allograft rejection in the absence of systemic immunosup

220 of IL-6 and IFN-gamma was upregulated during allograft rejection in untreated wild-type mice.

221 There were significantly more renal allograft rejections in the sensitized group (5 vs. 1; P

222 ere the critical effector mechanism of renal allograft rejection induced by memory CD4 T cells.

223 d CD8 T cells also did not prevent the renal allograft rejection induced by memory helper T cells sta

224 mma neutralization did not prevent the renal allograft rejection induced by memory helper T cells, an

225 of the potential mechanisms in tissue-organ allograft rejection involves the induction of granzymes

226 ked, and conversely how a system works where allograft rejection is a desired outcome rather than an

227 Chronic allograft rejection is a major impediment to long-term t

228 , and contrary to expectations, we find that allograft rejection is accelerated in KO recipients of M

229 nsplant models, the authors demonstrate that allograft rejection is accelerated in mice with a normal

230 ducts, alloantibodies-in the pathogenesis of allograft rejection is accepted.

231 Antibody-mediated allograft rejection is an increasingly recognized proble

232 Chronic lung allograft rejection is associated with a progressive for

233 unosuppressive reagents for preventing islet allograft rejection is associated with severe complicati

234 Allograft rejection is frequent in the 2 years after cor

235 Renal allograft rejection is more frequent under belatacept-ba

236 Allograft rejection is one of several undesirable conseq

237 Allograft rejection is one of the main obstacles for isl

238 Chronic lung allograft rejection is the single most important cause o

239 n, the exact role of IL-21 in the process of allograft rejection is unknown.

240 mental models of ulcerative colitis and lung allograft rejection led us to test the effect of the PHI

241 The profound involvement of cytokines in allograft rejection makes the molecules that control the

242 The fact that chronic allograft rejection may exist as early as 3 months after

243 Our study suggests that allograft rejection may not be an acute event, but rathe

244 ade of OX40-OX40L interactions prevents skin allograft rejection mediated by either subset of T cells

245 In this study, a murine acute renal allograft rejection model was used to investigate whethe

246 ations after transplantation include chronic allograft rejection, nephrotoxicity from calcineurin inh

247 Within 10 years, 4% of eyes developed allograft rejection, no primary graft failures occurred,

248 sly described in vivo effects on bone marrow allograft rejection observed with anti-Ly49A treatment i

249 transplantation, we demonstrated that acute allograft rejection occurred equally in MyD88-sufficient

250 Secondary outcomes included acute allograft rejection, opportunistic infections, graft and

251 according to underlying pathology into acute allograft rejection or AKI of other cause.

252 tended prophylaxis targeting recipients with allograft rejection or CMV infection may reduce the risk

253 liferation in naive mice and did not prevent allograft rejection or colitis.

254 No difference was found in allograft rejection or death between sirolimus-treated a

255 m rs1050501 affected susceptibility to renal allograft rejection or loss and transplant recipient sur

256 dministration in rats, and prevented corneal allograft rejection over the entire 9-week study when ad

257 ses (P = .005), diabetes mellitus (P = .03), allograft rejection (P = .001), CMV infection (P = .001)

258 ert different effects on mechanisms of renal allograft rejection, particularly at the level of Tfh ce

259 he effect of complement inhibition on kidney allograft rejection phenotype and the clinical response

260 ciated with a specific histomolecular kidney allograft rejection phenotype that can be abrogated by c

261 In a human-mouse chimeric model of allograft rejection, rapamycin pretreatment of human art

262 Biopsy-proven allograft rejection rate increased after month 12 in PRA

263 periodate-oxidized ATP [oATP]) delays islet allograft rejection, reduces the frequency of Th1/Th17 c

264 more accurate, noninvasive methods to detect allograft rejection remain an ongoing challenge.

265 Donor organ shortage and allograft rejection remain major limitations with only a

266 the use of immunosuppressive drugs, chronic allograft rejection remains a major hurdle in transplant

267 Allograft rejection remains a major source of morbidity

268 ne response toward the development of kidney allograft rejection remains unclear.

269 responses, their respective contribution to allograft rejection remains unclear.

270 Primary graft dysfunction and allograft rejection represent major caveats to successfu

271 plete antitumor response and T cell-mediated allograft rejection requiring reinitiation of hemodialys

272 ttransplantation for assessment of the acute allograft rejection response.

273 s of dd-cfDNA and correlated the levels with allograft rejection status ascertained by histology in 1

274 easured in urinary cells and correlated with allograft-rejection status with the use of logistic regr

275 licly and from our Genomics of Chronic Renal Allograft Rejection study.

276 chment requiring rebubbling in 5 eyes (22%), allograft rejection successfully reversed with topical s

277 clodronate-liposomes protects hearts against allograft rejection, suggesting a potential therapeutic

278 The non-HLAabs group had a higher rate of allograft rejection than controls (80% vs 55%), especial

279 l avenues for the treatment or prevention of allograft rejection that complement contemporary immunos

280 ed interplay between specific mRNA/miRNAs in allograft rejection that drive both immune-mediated inju

281 gs describe a distinct late phase of corneal allograft rejection that is likely mediated by Th17 cell

282 ncreasingly recognized to contribute to lung allograft rejection, the significance of endogenous inna

283 myocardium, cardiac fibrosis due to chronic allograft rejection up to 15 years after transplantation

284 ate T cell reconstitution and initiate heart allograft rejection upon adoptive transfer into mATG tre

285 activate murine MDSC capable of suppressing allograft rejection upon adoptive transfer.

286 10 displayed no significant features of skin allograft rejection upon histological analysis at 70 day

287 , we investigated the role of TLR4 in kidney allograft rejection using a fully major histocompatibili

288 of BLyS-directed immunotherapy in preventing allograft rejection using a murine islet transplantation

289 Mechanistically, Th2-mediated allograft rejection was contingent on IL-4, as its neutr

290 Allograft rejection was defined as International Society

291 Acute kidney allograft rejection was modestly attenuated in TLR4 mice

292 use these immune cells are involved in islet allograft rejection, we hypothesized that transplantatio

293 transplantation; A/H antigen expression and allograft rejection were assessed in graft biopsies.

294 = 0.0014), as well as the diagnosis of acute allograft rejection, which is preceded by increased immu

295 are being explored to mitigate memory driven allograft rejection, will also be reviewed.

296 Our algorithm predicts heart and lung allograft rejection with an accuracy that is similar to

297 Vehicle-treated rats developed severe allograft rejection with massive macrophage and T-cell i

298 f checkpoint inhibitors and the high risk of allograft rejection with their use.

299 This regimen effectively prevents allograft rejection without using steroids or calcineuri

300 r protein is an important mediator of kidney allograft rejection, yet the precise role of MyD88 signa