ライフサイエンスコーパス: graft rejection

1 primary endpoint 'time to first endothelial graft rejection'.

2 in hopes of reducing relapse and decreasing graft rejection.

3 y cross-react with allogeneic Ags to mediate graft rejection.

4 engraftment and more efficacy in controlling graft rejection.

5 ith fewer deaths resulting from GvHD or from graft rejection.

6 pressive medications administered to prevent graft rejection.

7 ferentiation after transplantation and rapid graft rejection.

8 logeneic non-self by monocytes in initiating graft rejection.

9 en associated with more risk for solid organ graft rejection.

10 mmunosuppression significantly reduced early graft rejection.

11 osuppressive treatment to prevent allogeneic graft rejection.

12 g therapy for T1D has been hampered by early graft rejection.

13 nomodulatory activity and its implication on graft rejection.

14 ications for the prevention and treatment of graft rejection.

15 ute to risk for opportunistic infections and graft rejection.

16 fers advantages in the form of lower risk of graft rejection.

17 led to induce tolerance but also accelerated graft rejection.

18 for the treatment of autoimmune diseases and graft rejection.

19 ltration of effector T cells, and ultimately graft rejection.

20 elopment of immunotherapies to prevent islet graft rejection.

21 usly other reasons than just pure allogeneic graft rejection.

22 trated to be markedly upregulated in corneal graft rejection.

23 bsequent procedures were not associated with graft rejection.

24 vation, differentiation, and the kinetics of graft rejection.

25 the CD8+ T effector cells requisite for skin graft rejection.

26 We identified 45 cases of graft rejection.

27 En/DM) characteristics in diagnosing corneal graft rejection.

28 o decades to reverse steroid-resistant acute graft rejection.

29 ell as in preventing autoimmune diseases and graft rejection.

30 may be useful for the treatment of vascular graft rejection.

31 per of T cell lineage development in cardiac graft rejection.

32 lation of MDSC can participate in preventing graft rejection.

33 ata, lifelong immunosuppression, and chronic graft rejection.

34 low the clinical and immunologic outcomes of graft rejection.

35 ter established tolerance resulted in prompt graft rejection.

36 allografts, and enable better prediction of graft rejection.

37 ut also alloantibody elaboration and chronic graft rejection.

38 y between alloimmunity and autoreactivity in graft rejection.

39 of transplantation abrogates protection from graft rejection.

40 ining and validating an imaging signature of graft rejection.

41 diators and accelerate T cell-meditated skin graft rejection.

42 n this study, irrespective of interval acute graft rejection.

43 cell transplantation to reduce immunological graft rejection.

44 ve therapeutic potential for T cell-mediated graft rejection.

45 drawal should be selected carefully to avoid graft rejection.

46 a viable therapeutic target to prevent acute graft rejection.

47 antileukemia effect and a lower incidence of graft rejection.

48 desensitization, and assessing the risk for graft rejection.

49 the direct T-cell infiltration that mediates graft rejection.

50 graft-versus-host disease (GVHD), and organ graft rejection.

51 ocompatibility complexes and thereby mediate graft rejection.

52 in the setting of myocardial dysfunction and graft rejection.

53 immunosuppressive therapies while preventing graft rejection.

54 aries between prevention of autotoxicity and graft rejection.

55 therapies while preventing acute and chronic graft rejection.

56 both CD8 T cell infiltration and acute skin graft rejection.

57 emokine action is of potential in preventing graft rejection.

58 CD8(+) T cell responses and precipitation of graft rejection.

59 t induce graft-versus-host disease (GVHD) or graft rejection.

60 ded on the Y-chromosome, in association with graft rejection.

61 nd reversed costimulation blockade-resistant graft rejection.

62 ls possibly influencing the intensity of the graft rejection.

63 nst both graft-versus-host disease and organ graft rejection.

64 d have been linked to immunosurveillance and graft rejection.

65 Alloreactive B cells can contribute to graft rejection.

66 ne response in the clinical setting of acute graft rejection.

67 CD8(+) cells, and macrophages at the time of graft rejection.

68 likely associated with T-cell expansion and graft rejection.

69 body of Sens(+)Chall(+) eyes at the time of graft rejection.

70 esis has been successfully used to attenuate graft rejection.

71 associated with an increased rate of corneal graft rejection.

72 in cases of bowel dysfunction not related to graft rejection.

73 s cross-react with allogeneic Ag and mediate graft rejection.

74 nd triggers BKPyV-associated nephropathy and graft rejection.

75 erative management and prevention of corneal graft rejection.

76 cell-specific IL-10 deficient mice prevented graft rejection.

77 cardiac allograft specimens undergoing acute graft rejection.

78 A at this time significantly reduced corneal graft rejection.

79 initiation of adaptive responses that cause graft rejection.

80 between groups were observed in the risk of graft rejection.

81 by the immunosuppression required to prevent graft rejection.

82 s a key event in triggering alloimmunity and graft rejection.

83 apeutic approaches to autoimmune diseases or graft rejections.

84 yte autoantibodies are associated with fewer graft rejections.

85 3 years after DSAEK and PKP were immunologic graft rejection (0.6% vs. 3.1%), endothelial decompensat

86 ons in these patients included glaucoma (1), graft rejection (1), recurrence of disease (1), and ambl

87 The complications noted in the patients were graft rejection (1), shield ulcers (2), graft infection

88 Thirty of 353 DSAEKs developed graft rejection (8.5%).

89 ine, or DSP in solution demonstrated corneal graft rejection accompanied by severe corneal edema, neo

90 erum creatinine concentrations and to kidney graft rejection after about a month.

91 Late graft rejection after conditioning with 1 Gy of total bo

92 Graft rejection after cryptococcosis was observed in 15.

93 at a physiological ratio were able to delay graft rejection after direct alloreactivity by controlli

94 The risk for graft rejection after DMEK is low, and an even smaller m

95 e of ECD loss with time in eyes experiencing graft rejection after DSAEK surgery.

96 Preformed host antibodies may contribute to graft rejection after hematopoietic stem-cell transplant

97 onstellation also predicted the incidence of graft rejection after liver and lung transplantation, wi

98 ular pathologies constitute a major cause of graft rejection after organ transplantation.

99 atment of autoimmune diseases and to prevent graft rejection after organ transplantation.

100 enesis and lymphangiogenesis, and suppressed graft rejection after transplantation.

101 mem) can play an important role in mediating graft rejection after transplantation.

102 eta cells is involved in beta cell death and graft rejection after transplantation.

103 ative total body irradiation prevented organ graft rejection, all hosts succumbed to lethal graft-ver

104 et-expressed antigens is prevented and islet graft rejection alleviated.

105 genes would explain why cheetahs ablate skin graft rejection among unrelated individuals.

106 is evidence that NK cells can contribute to graft rejection and also to tolerance induction.

107 ished models of acute and chronic intestinal graft rejection and analyzed peripheral and intragraft i

108 lung transplantation despite the absence of graft rejection and cardiac dysfunction.

109 recipient age, African American race, acute graft rejection and CMV infection were significantly ass

110 number of TIM-3+ Tregs peaked at the time of graft rejection and declined thereafter.

111 inhibition of JAK3 has been shown to prevent graft rejection and decrease the severity of arthritis i

112 the involvement of Langerhans cells in skin graft rejection and describe fascinating results.

113 tigenic targets that have been implicated in graft rejection and discuss the interplay between alloim

114 g H-Y incompatibility, on corneal transplant graft rejection and failure.

115 nt seroconstellation remains associated with graft rejection and graft loss in the era of prophylacti

116 Graft rejection and graft-versus-host disease (GVHD) are

117 sphamide after transplantation inhibits both graft rejection and graft-versus-host disease (GvHD) in

118 apa cells skewed toward a Th2-type prevented graft rejection and graft-versus-host disease (GVHD) mor

119 -transplantation cyclophosphamide to prevent graft rejection and graft-versus-host disease (GVHD).

120 ogeneic stem-cell transplantation to prevent graft rejection and graft-versus-host disease (GvHD).

121 in from day -5 to -3 was used for preventing graft rejection and graft-versus-host disease (GVHD); no

122 egrees of preparative regimen intensity, but graft rejection and graft-vs-host disease remain signifi

123 se studies suggest that ICOS plays a role in graft rejection and GVHD in an outbred animal model, and

124 Anti-E-selectin treatment delayed graft rejection and increased survival compared with con

125 on; one died at 183 days as a consequence of graft rejection and infection.

126 teroid avoidance appears safe with regard to graft rejection and loss in pediatric kidney transplant

127 H60 incompatibility does not result in skin graft rejection and only a minority of heart transplants

128 ng infection, cancer, autoimmunity, allergy, graft rejection and other immunological processes.

129 ve ALS and 21 days CsA significantly delayed graft rejection and promoted long-term (>125 days) graft

130 T(reg) cells leads to autoimmune disease and graft rejection and promotes anti-tumor immunity.

131 tivation (including opportunistic infection, graft rejection and severe hepatitis C virus recurrence)

132 ations of bone marrow transplants, including graft rejection and the chronic immunosuppression requir

133 ) regulatory T cells (nTregs) in controlling graft rejection and the mechanism used remain controvers

134 ithin the hematopoietic compartment leads to graft rejection and therapeutic failure because of antig

135 sed at a physiological ratio failed to delay graft rejection and to control proliferation of conventi

136 Investigations in diverse areas, including graft rejection and tolerance, autoimmunity and infectio

137 lassemia is challenging due to high rates of graft rejection and transplant-related mortality.

138 f CCL22 could be harnessed for prevention of graft rejection and type 1 diabetes as well as other aut

139 tal tool for timely prevention of intestinal graft rejection and, more important, avoidance of overim

140 e, the result may be a situation that favors graft rejection and/or makes tolerance difficult to achi

141 or source of pathogenic Abs in autoimmunity, graft rejection, and allergy.

142 ization, cellular and molecular mediators of graft rejection, and allotolerance induction.

143 sed in the treatment of autoimmune diseases, graft rejection, and cancer.

144 ma includes withdrawal of immunosuppression, graft rejection, and explantation of the allograft after

145 on of rare SNPs in malignancy, monitoring of graft rejection, and fetal screening.

146 We correlated CMV infection, biopsy-proven graft rejection, and graft loss in 1,414 patients receiv

147 f autoimmune diseases, for the prevention of graft rejection, and graft versus host disease.

148 orm in chronic inflammation in autoimmunity, graft rejection, and microbial infection.

149 to the recruitment of inflammatory cells for graft rejection, and modulation of chemokine action is o

150 arization, need for transplantation, risk of graft rejection, and QoL.

151 s are nonspecific and occur in pancreatitis, graft rejection, and subsequent graft ischemia.

152 recipients is sufficient to directly mediate graft rejection, and the absence of recipient CCR5 expre

153 ration of immunosuppressive drugs to prevent graft rejection, and these agents may significantly limi

154 strike implies a central role for B cells in graft rejection, and this approach may help to delay or

155 However, concerns about relapse, graft rejection, and variability in technique have limit

156 munosuppression, which increases the risk of graft rejection, anti-CD20 treatment, combination chemot

157 Rates of graft rejection are high among recipients of heart trans

158 ive thickening of the En/DM is diagnostic of graft rejection as measured by DMT and DRI.

159 tegy and could be used both to prevent acute graft rejection as well as for maintenance immunosuppres

160 exacerbated ischemia/reperfusion injury and graft rejection, as demonstrated by increased myocardial

161 r anti-CD200R1/R2 monoclonal antibody caused graft rejection, as did anti-interleukin (IL)-9, anti-IL

162 ning the biological pathways responsible for graft rejection at the molecular level and identifying g

163 we found a trend toward a lower incidence of graft rejection at year 1 in the "monitoring" group (30.

164 Most early PTLD patients experienced graft rejection before PTLD diagnosis (P=0.0081).

165 Incidence of graft rejection, best spectacle-corrected visual acuity

166 osporine, markedly attenuated not only acute graft rejection but also alloantibody elaboration and ch

167 Immunosuppression prevents graft rejection but seems to accelerate the recurrence o

168 odies (DSA) are associated with acute kidney graft rejection, but their role in small bowel/multivisc

169 autoimmune diseases, allergic disorders, and graft rejection by depleting undesired disease-causing T

170 Post-transplant immune complications include graft rejection by the host and injury to the host media

171 CNI reduction and elimination, and risk for graft rejection; (C) antiproliferative effects of EVR; a

172 However, graft rejection can occur long after a state of transpla

173 g risk factors traditionally associated with graft rejection, cessation of topical steroids was most

174 posttransplant mortality, graft loss, acute graft rejection, chronic rejection, cancer, infection, a

175 Outcome measures included rates of graft rejection, clinical findings, treatment outcomes,

176 pecific Tregs offers greater protection from graft rejection compared to polyclonal Tregs.

177 nhibition or even acceleration of donor skin graft rejection compared with non-DST control (naive) bm

178 effects on hemodynamically significant/fatal graft rejection, coronary vasculopathy, terminal cancer,

179 (+) T cells to approximately 5% precipitated graft rejection despite CD28/CD154 blockade.

180 ourse of autoimmune, infectious, and chronic graft rejection diseases, in which a sustained lymphocyt

181 dney graft function, TrBs from patients with graft rejection displayed similar IL-10 expression level

182 Furthermore, NK cell-mediated graft rejection does not show features of memory respons

183 btly yet reproducibly decreases time to skin graft rejection elicited by central but not effector mem

184 A graft rejection episode developed in 12 patients (estima

185 Eyes with a graft rejection episode had a higher median percentage d

186 Patients with a graft rejection episode were followed up for 1 additiona

187 analyze the incidence and clinical course of graft rejection episodes after Descemet membrane endothe

188 Patients with graft rejection episodes and late endothelial failure we

189 (<1%) cumulative probability of immunologic graft rejection episodes through 2 years after DMEK.

190 Graft rejection episodes were seen in 5 eyes (12.1%) in

191 splant recipients is a major risk factor for graft rejection episodes, and it has significant financi

192 t all time points compared with eyes without graft rejection episodes.

193 The incidence of graft-rejection episodes is lower after DSEK compared wi

194 elease of corticosteroids to prevent corneal graft rejection following subconjunctival injection prov

195 Graft rejection has been defined as the mirror image of

196 ho are medically immunosuppressed to prevent graft rejection, have increased melanoma risk, but risk

197 ioning and immunologic phenomena ascribed to graft rejection hence prolong islet allograft survival.

198 mune disease, inflammatory bowel disease and graft rejection, however the mechanisms by which they ca

199 Since HLA antibody is a potential cause of graft rejection, identifying the epitope-or antigenic de

200 In a setting of CD8(+) cell-dominant graft rejection, IL-6 neutralization delayed the onset o

201 ion, but to correlate these methods to early graft rejection, immunobiologic techniques will probably

202 trophils, were confirmed by third-party skin graft rejection; importantly, a graft-versus-leukemia as

203 at had rejected corneal allografts, produced graft rejection in 70% and 20% of the hosts, respectivel

204 d gene transfer of thymosin beta4 attenuated graft rejection in a heterotopic heart transplantation m

205 er Th2 cells alone accounted for accelerated graft rejection in allergic mice.

206 ction by alloprimed IgG1 B cells and delayed graft rejection in both low and high alloantibody produc

207 has been associated with atherosclerosis and graft rejection in heart transplant recipients.

208 sure to conventional therapies in preventing graft rejection in high-risk corneal transplantation.

209 Importantly, blockade of TNFR2 attenuated graft rejection in low- but not high-affinity-primed ani

210 to directly alloreactive T cells and delayed graft rejection in mice.

211 hibitor Rapamycin, could significantly delay graft rejection in one mouse strain, and achieve transpl

212 ntibodies are associated with a high rate of graft rejection in patients undergoing haploidentical st

213 While CsA has been widely used to prevent graft rejection in patients undergoing organ transplant

214 tigated the putative candidate biomarkers of graft rejection in peripheral blood of intestinal transp

215 ion alone has proven insufficient to prevent graft rejection in primates.

216 therapy targeting CD4 and CD154 to overcome graft rejection in sensitized recipients.

217 LA) antibodies (DSA) have been implicated in graft rejection in solid organ transplantation, their ro

218 In addition, the biopsy could rule out graft rejection in the atypical subjects who had oligocl

219 s to develop a pre-clinical model of corneal graft rejection in the semi-inbred NIH minipig as a mode

220 TBI was well tolerated but failed to prevent graft rejection in this model.

221 In this study, we examined graft rejection in three mouse models: 1) mismatch of ma

222 nce cancer metastasis and accelerate chronic graft rejection in transplant recipients.

223 of microchimerism in predicting the risk of graft rejection in transplantation.

224 vitro Ag-specific Foxp3(+) nTregs to control graft rejection in transplantation.

225 f pTregs from mice at low risk of subsequent graft rejection is able to rescue graft survival in reci

226 Graft rejection is an important complication following D

227 hus, allergy-induced exacerbation of corneal graft rejection is due to the production of IL-4, which

228 RESULT: CD4 T cell-mediated cardiac graft rejection is inhibited using RIP3 deficient donor

229 organs, withdrawal of immunosuppression and graft rejection is not feasible, and reduction of immuno

230 Immunologic graft rejection is one of the main causes of short and l

231 nocytes and macrophages contribute to kidney graft rejection is poorly understood.

232 responses in vivo, as demonstrated by faster graft rejection kinetics and greater proliferative respo

233 -modified DCs prior to transplantation, skin graft rejection kinetics were similar to those in non-DC

234 In this study, we examined the graft-rejection kinetics and CD4(+) and CD8(+) donor-rea

235 One graft rejection leading to graft failure was seen and wa

236 There were no differences in rates of graft rejection, leukemia relapse, treatment-related mor

237 A graft rejection-like program occurs in the ZAM, which in

238 n with associated complications, and chronic graft rejection, limit its wide clinical application.

239 the required frequency of dosing for corneal graft rejection management can be as high as once every

240 transplantation in patients, irrespective of graft rejection, may be high at the time of humoral reje

241 upregulated on memory T cells, did not delay graft rejection mediated by CXCR3 memory T cells.

242 patients can develop an accelerated form of graft rejection mediated by humoral and T-cell-mediated

243 In a B6-into-BALB/c graft rejection model, donor Th2/Tc2.R cells were indeed

244 ntidonor T cell priming in a MyD88-dependent graft rejection model.

245 The increased graft rejection observed in conventional animals was due

246 estricted to a single foreign antigen on the graft, rejection occurred only if the allogeneic non-sel

247 otypic differences are capable of triggering graft rejection of an organ transplanted between identic

248 There was one episode of graft rejection on belatacept therapy in a patient who h

249 need to better understand the mechanisms of graft rejection or acceptance.

250 y up-regulated on T cells in dogs undergoing graft rejection or chronic GVHD after allogeneic hematop

251 is multifactorial and can be an indicator of graft rejection or coronary artery vasculopathy.

252 Main outcome measures were graft rejection or failure at 5 years.

253 by T cell-mediated alloresponses that cause graft rejection or graft-versus-host disease.

254 No additional graft rejection or GvHD prophylaxis was given.

255 of anti-donor T cells during elicitation of graft rejection or induction/maintenance of transplant t

256 6; 95% CI: 1.04-339.37; p = 0.047) and acute graft rejection (OR: 40.73, 95% CI: 3.63-456.98; p = 0.0

257 matological complications and graft failure, graft rejection, or death.

258 umulative incidence of complications such as graft rejection (P < 0.001), epitheliopathy (P < 0.001),

259 Graft rejection, patient survival, and non-CMV infection

260 to revise the clinical perspective on acute graft rejection, pending the results of larger studies.

261 rticosteroids may reduce the rate of corneal graft rejection, perhaps especially in the days immediat

262 that subsequent to T cell initiation of skin graft rejection, platelets contribute to further T cell

263 Risk of graft rejection, postoperative complication, and late EC

264 In conclusion, T cell-mediated marrow graft rejection primarily resembles a Th1-type process t

265 rer immune recovery and in increased risk of graft rejection, pure hematopoietic stem cells (HSC), wh

266 Despite favorable outcomes, immune-mediated graft rejection remains the major cause of corneal allog

267 within allografts, but their contribution to graft rejection remains unclear.

268 fic induction of SENP1 and GATA2 in clinical graft rejection specimens that show endothelial activati

269 al blood mononuclear cells and plasma during graft rejection suggesting potential as a biomarker of g

270 o prime alloreactive T cells and accelerated graft rejection, suggesting that alloimmunity is modulat

271 east as poorly as those with reported kidney graft rejection supporting the concept of concordance of

272 an MHC class I alloantigen, the accelerated graft rejection T memory response is specifically lost s

273 be the gold standard in diagnosing pancreas graft rejection, they are not performed routinely becaus

274 B cells have been reported to promote graft rejection through alloantibody production.

275 s toward the main effector cells involved in graft rejection through inhibition of natural killer cel

276 ects of PPARgamma agonists on human vascular graft rejection using a model in which human artery is i

277 Thus, our results suggest the paradigm that graft rejection versus tolerance is determined by a bala

278 ze allogeneic entities and that they mediate graft rejection via direct cytotoxicity and priming of a

279 llow-up was 26 months (range, 12-62 months); graft rejection was 10%.

280 On the other hand, the median time to graft rejection was 28 +/- 5.2 days and 16 +/- 2.6 days

281 mmaRIIb-mediated inhibition of B6.K(d) heart graft rejection was abrogated by increasing T cell help

282 were acutely rejected within 10-13 days and graft rejection was associated with increased frequencie

283 Graft rejection was associated with the development of e

284 Graft rejection was defined as findings of keratic preci

285 o maintain therapeutic levels; no episode of graft rejection was observed during the study.

286 pients; ribavirin did not influence SVR, and graft rejection was rare.

287 Graft rejection was seen in one autopsy.

288 Risk factors for development of graft rejection were cessation of postoperative steroid

289 rejection, chronic renal rejection, and skin graft rejection were compared using CD20 or CD19 mAbs.

290 No episodes of immunologic graft rejection were documented.

291 Risk factors for graft rejection were reviewed.

292 hways, we used a single-Ag mismatch model of graft rejection where we could track the donor-specific

293 (anti-CD3 mAb) and found it could delay skin graft rejection, whereas ipilimumab (anti-CTLA-4 [cytoto

294 Inductive OX40 stimulation induced acute graft rejection, which correlated with both IgG1 and IgG

295 perative injuries to an allograft exacerbate graft rejection, which in humans is primarily mediated b

296 elevated MDC:PDC ratio associates with liver graft rejection, which occurs after first year in childr

297 on that has been linked to renal and cardiac graft rejection, which was originally thought to be Th1-

298 In models of vaccination and allogeneic graft rejection, whole body imaging reveals that RA sign

299 were at an increased risk for biopsy-proven graft rejection within 4 weeks after detection of CMV re

300 As such, we reasoned that graft rejection would represent a Th1 response amenable