ライフサイエンスコーパス: transplant rejection

1 ecule may promote inflammatory responses and transplant rejection.

2 eg-dependent suppression of autoimmunity and transplant rejection.

3 ted disorders such as autoimmune disease and transplant rejection.

4 r treatment of autoimmune diseases and organ transplant rejection.

5 nt role in characterization and treatment of transplant rejection.

6 ction between molecules with a known role in transplant rejection.

7 dominant pathway of allorecognition in acute transplant rejection.

8 role in the development of inflammation and transplant rejection.

9 mplex class II alloantigens to suppress skin transplant rejection.

10 contrasts with their prominent role in organ transplant rejection.

11 fluence of host and donor microbiota on skin transplant rejection.

12 Th17 phenotype has prompted its scrutiny in transplant rejection.

13 ccessful as cyclosporin in suppressing organ transplant rejection.

14 t role for platelets in alloantibody induced transplant rejection.

15 in the treatment of autoimmune diseases and transplant rejection.

16 hy and, in particular, alloantibody-mediated transplant rejection.

17 mune and inflammatory disorders and/or organ transplant rejection.

18 type V collagen [col(V)] contributes to lung transplant rejection.

19 schemic reperfusion injury (IRI), and tissue transplant rejection.

20 une and allergic diseases, or for preventing transplant rejection.

21 activation of exocytosis may play a role in transplant rejection.

22 mage, including vascular disease and chronic transplant rejection.

23 antigens" responsible for antibody-mediated transplant rejection.

24 ll antibodies used clinically to treat acute transplant rejection.

25 immunosuppressant developed to prevent organ transplant rejection.

26 mune and inflammatory disorders and/or organ transplant rejection.

27 ying the common component C4 in mouse kidney transplant rejection.

28 ce of immunosuppression, to T cell-dependent transplant rejection.

29 allogeneic MHC complexes is a major cause of transplant rejection.

30 ole in a variety of autoimmune disorders and transplant rejection.

31 in intrarenal oxygenation occur during acute transplant rejection.

32 alignancies, autoimmune disease, and humoral transplant rejection.

33 ers such as autoimmune disease and allograft transplant rejection.

34 oma components, and microbubbles for imaging transplant rejection.

35 be a novel molecular target for controlling transplant rejection.

36 r necrosis factor alpha (TNF-alpha) in liver transplant rejection.

37 ung diseases such as asthma and chronic lung transplant rejection.

38 ch as autoimmunity, anti-tumor immunity, and transplant rejection.

39 ve drug that is widely used to prevent organ transplant rejection.

40 s in endomyocardial biopsy samples to assess transplant rejection.

41 causal relationship between alloantibody and transplant rejection.

42 ost, including vascular diseases and chronic transplant rejection.

43 therapeutic potential for the prevention of transplant rejection.

44 rogenic population to treat autoimmunity and transplant rejection.

45 cer, autoimmune and infectious diseases, and transplant rejection.

46 ng clinical trials to combat immune-mediated transplant rejection.

47 nity, it remains unstudied in the context of transplant rejection.

48 heumatoid arthritis, multiple sclerosis, and transplant rejection.

49 immunity and the amelioration of allogeneic transplant rejection.

50 human kidney and their altered expression in transplant rejection.

51 xposures to cyclosporine to prevent pancreas-transplant rejection.

52 me Fe-S cluster protein in acute solid organ transplant rejection.

53 er number (3 x 10(6)) was required for heart transplant rejection.

54 human conditions, including autoimmunity and transplant rejection.

55 rteries, in parallel with SODD, during acute transplant rejection.

56 teract during allogeneic encounters and thus transplant rejection.

57 A, represents an ideal strategy for reducing transplant rejection.

58 calcineurin and block T-cell activation and transplant rejection.

59 atment of autoimmune diseases and to prevent transplant rejection.

60 RA mRNA up-regulation as a marker for kidney transplant rejection.

61 promise in dampening allergic reactions and transplant rejection.

62 ons to treat cancer, and HIV, and to prevent transplant rejection.

63 RNA expression in blood during human corneal transplant rejection.

64 for the treatment of autoimmune disease and transplant rejection.

65 with in vitro IFNgamma production and renal transplant rejection.

66 Fas mRNA in blood may have a role in corneal transplant rejection.

67 can be targeted for noninvasive detection of transplant rejection.

68 and is a prominent feature of chronic renal-transplant rejection.

69 ction, juvenile chronic arthritis, and renal transplant rejection.

70 tivity, have implicated these eicosanoids in transplant rejection.

71 trate a role for CXCR3 in the development of transplant rejection.

72 a major aim for therapy in autoimmunity and transplant rejection.

73 for the treatment of autoimmune diseases or transplant rejection.

74 is provided has not been fully delineated in transplant rejection.

75 terns in different morphological patterns of transplant rejection.

76 the indirect pathway is involved in chronic transplant rejection.

77 uppression decreases the rate of acute renal transplant rejection.

78 s like RANTES appear to play a role in organ transplant rejection.

79 urine monoclonal antibodies for treatment of transplant rejection.

80 sitive for the detection of acute pancreatic transplant rejection.

81 ted for treatment of autoimmune diseases and transplant rejection.

82 eatment of leukaemia, autoimmune disease and transplant rejection.

83 that may play a significant role in cardiac transplant rejection.

84 d arthritis, autoimmune diabetes, or chronic transplant rejection.

85 autoantibodies in patients at high risk for transplant rejection.

86 Australia convened in 1995 to examine kidney transplant rejection.

87 ting both human autoimmune disease and organ transplant rejection.

88 strategies to prevent autoimmune disease and transplant rejection.

89 es of several glomerular diseases, including transplant rejection.

90 cell responses involved in autoimmunity and transplant rejection.

91 are critical for, the development of chronic transplant rejection.

92 umatoid arthritis, gout, sepsis, stroke, and transplant rejection.

93 on of an intervening episode of severe acute transplant rejection.

94 infarction, hypertension, heart failure, and transplant rejection.

95 tentially modulate inflammatory reactions or transplant rejection.

96 n is a common feature of cell-mediated renal transplant rejection.

97 terfere with the T-cell signals important in transplant rejection.

98 essive agent used for the treatment of acute transplant rejection.

99 esponses, including autoimmune disorders and transplant rejection.

100 treat T cell-mediated pathologies, including transplant rejection.

101 to the heart during inflammation and cardiac transplant rejection.

102 and/or ameliorating autoimmune diseases and transplant rejection.

103 ated T-cell costimulation and prevents renal transplant rejection.

104 a target for the prevention and treatment of transplant rejection.

105 nsitive and quantitative diagnostic test for transplant rejection.

106 ant model was used to study NK cell-mediated transplant rejection.

107 graft tolerance dominates over the memory of transplant rejection.

108 lex alleles, the most potent determinants of transplant rejection.

109 ene transcripts to refine diagnosis of heart transplant rejection.

110 hways may also contribute to pathogenesis of transplant rejection.

111 ls became activated, ultimately resulting in transplant rejection.

112 d autoimmune disease, cancer, infection, and transplant rejection.

113 t is particularly important in infection and transplant rejection.

114 for pathogen surveillance, autoimmunity, and transplant rejection.

115 clinical consequence of treatment to prevent transplant rejection.

116 increased memory T cells, which may promote transplant rejection.

117 ine interleukin-17, which has been linked to transplant rejection.

118 herapies of inflammatory kidney diseases and transplant rejection.

119 t include degenerative diseases, cancer, and transplant rejection.

120 erived components as immune suppressants for transplant rejection.

121 toimmunity, as well as for the prevention of transplant rejection.

122 ion secondary to infection, inflammation, or transplant rejection.

123 sorders including autoimmunity, allergy, and transplant rejection.

124 T cells and contributes to T cell-dependent transplant rejection.

125 immunity, dermatitis, periodontitis and even transplant rejection.

126 hat is a leading reflection of chronic heart transplant rejection.

127 mph nodes and beyond and also promotes organ transplant rejection.

128 s of hIL-10-TFLs are efficient in mitigating transplant rejection.

129 toimmune and allergic responses, and prevent transplant rejection.

130 ree lymphangiogenesis in mediating high-risk transplant rejection.

131 hemical insults and is a primary mediator of transplant rejection.

132 l binding partner for PDL1 other than PD1 in transplant rejection.

133 n was restricted to patients at low risk for transplant rejection; among high-risk patients, alemtuzu

134 une-mediated tissue injury following cardiac transplant rejection, an in vivo model of intense inflam

135 of human organ-specific autoimmune diseases, transplant rejection and allergic diseases.

136 ells are significant mediators of hepatocyte transplant rejection and are relatively resistant to cos

137 ainst the alpha1(V) chain are linked to lung transplant rejection and atherosclerosis.

138 lective immunosuppressive agents to mitigate transplant rejection and autoimmune diseases requires ef

139 uction could also enable novel therapies for transplant rejection and autoimmune diseases.

140 of CD28, under development for treatment of transplant rejection and autoimmune diseases.

141 ght prove to be important for the therapy of transplant rejection and autoimmune diseases.

142 fer and more convenient treatments for organ transplant rejection and autoimmune disorders such as rh

143 and discuss implications for T-cell mediated transplant rejection and autoimmune disorders.

144 Th cells are the major effector cells in transplant rejection and can be divided into Th1, Th2, T

145 e latter five demonstrated at least moderate transplant rejection and caspase-3 staining, suggesting

146 AP between patients at high risk for corneal transplant rejection and control subjects (P<0.001).

147 le of resident versus circulating T cells in transplant rejection and in providing protection to prev

148 t the AHR and will have efficacy in treating transplant rejection and in tolerance protocols.

149 stigated, despite the increased incidence of transplant rejection and inferior allograft outcomes in

150 ney transplant recipients who develop severe transplant rejection and malignant hypertension during t

151 ancers, autoimmune disorders, infection, and transplant rejection and may help to design better vacci

152 e (OIH), can be used to identify acute renal transplant rejection and measure its severity.

153 ed to study the role of human macrophages in transplant rejection and other pathologies in vivo.

154 technique for the detection of acute cardiac transplant rejection and other processes characterized b

155 ping immunotherapeutic approaches to inhibit transplant rejection and potentially other immune-mediat

156 Nanoparticle macrophage PET-CT detects heart transplant rejection and predicts organ survival by repo

157 Allograft loss was associated with chronic transplant rejection and recurrence of lupus nephritis.

158 l (Treg) therapy is a promising approach for transplant rejection and severe autoimmunity.

159 lation was also identified between high-risk transplant rejection and severe lymphatic invasion reach

160 HLA variation is a crucial determinant of transplant rejection and susceptibility to a large numbe

161 a target for autoimmunity disorders, tissue transplant rejection and T-cell malignancies.

162 We hypothesize that prolonged T2 reflects transplant rejection and that quantitative T2 mapping wi

163 loreactive plasma cells in acute Ab-mediated transplant rejection and their autoreactive counterparts

164 d to better understand mechanisms underlying transplant rejection and tolerance in humans.

165 reactivity will help elucidate mechanisms of transplant rejection and tolerance in vivo.

166 nting cells (APCs) play an important role in transplant rejection and tolerance.

167 for the treatment of autoimmune diseases and transplant rejection and toward modification of tumor im

168 IL2 production and is widely used to prevent transplant rejection and treat autoimmunity.

169 of such diverse diseases as atherosclerosis, transplant rejection and tumor-related angiogenesis.

170 For living donor transplants, rejection and graft survival rates are rela

171 ogenous CO protects against vascular injury, transplant rejection, and acute lung injury.

172 ) Treg for treatment of autoimmune diseases, transplant rejection, and allergy.

173 allograft survival in vivo, prevents corneal transplant rejection, and attenuates the progression and

174 certain cancers, autoimmune disorders, organ transplant rejection, and bowel disease.

175 nct sensitivity to growth factor blockade in transplant rejection, and CD28/CD154-independent rejecti

176 injury, end-stage renal failure, acute renal transplant rejection, and delayed allograft function.

177 ated conditions such as autoimmune diseases, transplant rejection, and graft-versus-host disease.

178 ctivity can attenuate autoimmunity and delay transplant rejection, and heat shock proteins derived fr

179 of chronic DC-triggered autoimmune diseases, transplant rejection, and hematologic malignancies with

180 expressed in a regulated manner during renal transplant rejection, and identify DR3 as a potential in

181 Inflammation in asthma, sepsis, transplant rejection, and many neurodegenerative disease

182 T cells can suppress graft-vs-host disease, transplant rejection, and MLRs.

183 de novel therapies for corneal inflammation, transplant rejection, and other lymphatic-related disord

184 potent but short-lived stimulators of early transplant rejection, and recipient antigen presenting c

185 such as atherosclerosis, malaria infection, transplant rejection, and rheumatoid arthritis.

186 dely recognized as playing a pivotal role in transplant rejection, and several studies have shown tha

187 tions, including arthritis, atherosclerosis, transplant rejection, and severe malaria.

188 rodegenerative states, organ and bone marrow transplant rejection, and tumor response to chemotherapy

189 's disease, diabetes, multiple sclerosis and transplant rejection appear to be the next burgeoning ph

190 ge-based diagnosis of acute allogeneic renal transplant rejection (AR) established in a rat model.

191 progression of clinically significant heart transplant rejection are currently monitored by serial b

192 asive techniques for detecting acute cardiac transplant rejection are limited.

193 ative contributions of these two pathways to transplant rejection are partially understood.

194 T cells resisting to CD28/CD154 blockade in transplant rejection are sensitive to OX40 blockade and

195 Current therapies for transplant rejection are suboptimally effective.

196 s, such as atherosclerosis acute and chronic transplant rejection, arthritis, influenza, and malaria

197 ons should have applications in treatment of transplant rejection as well as autoimmune diseases.

198 onged xenograft survival and is important in transplant rejection as well.

199 Therapy for transplant rejection, autoimmune disease and allergy mus

200 nt sites, as well as its known role in organ transplant rejection, autoimmune disease development and

201 modulator of inflammatory diseases including transplant rejection, autoimmunity, and allergy.

202 d, has clinical utility for the treatment of transplant rejection based on its inhibition of IMPDH.

203 Bortezomib in Late Antibody-Mediated Kidney Transplant Rejection [BORTEJECT] Trial), we investigated

204 Hence, CNIs not only prevent organ transplant rejection but also contribute to the developm

205 globulin (Thymoglobulin) effectively treats transplant rejection but induces anti-rabbit Ab response

206 oduces clinical immunosuppression preventing transplant rejection but is associated with transient br

207 ng effector mechanisms associated with acute transplant rejection but that it is required for initiat

208 cognized as a contributor to inflammation in transplant rejection but without detailed analysis of it

209 Platelets have been described as markers of transplant rejection, but little investigation has criti

210 elets have been long described as markers of transplant rejection, but the contribution of platelets

211 the adaptive immune system are critical for transplant rejection, but the role of the innate immune

212 the transplanted kidney are known to mediate transplant rejection, but which of the three main activa

213 Clinical detection of transplant rejection by repeated endomyocardial biopsy r

214 may improve autoimmune diseases and prevent transplant rejection by suppressing the differentiation

215 nexin-V imaging for noninvasive detection of transplant rejection by targeting cell membrane phosphol

216 Adjustment for known risk factors for transplant rejection confirmed the univariate findings f

217 ated inhibition of alloresponses involved in transplant rejection correlates with CD86 saturation, in

218 During allergy, autoimmunity and transplant rejection, DCs instigate unwanted responses t

219 ggest that while alloimmunity initiates lung transplant rejection, de novo autoimmunity mediated by c

220 HHV-6 reactivation has been associated with transplant rejection, delayed engraftment, encephalitis,

221 hangiogenesis mediates diseases like corneal transplant rejection, dry eye disease, and allergy.

222 plicated in costimulation blockade-resistant transplant rejection, due to their enhanced effector fun

223 causal relationship between alloantibody and transplant rejection-especially chronic rejection-has be

224 Instead, transplant rejection following LM infection was dependen

225 diseases, ranging from cancer metastasis to transplant rejection, for which there is little effectiv

226 At 6 months, kidney transplant rejection had occurred in 38% of BD PTx vs. 3

227 Transplant rejection has generally been considered a CD4

228 ection, but the contribution of platelets to transplant rejection has not been critically examined.

229 of TNF-R1-mediated signaling in solid organ transplant rejection has not been defined.

230 suppressant used for the prevention of renal transplant rejection, has recently emerged as an effecti

231 tes numerous immunologic effects relevant to transplant rejection; however, its specific contribution

232 diovascular diseases including acute cardiac transplant rejection; however, the contribution of ECM-d

233 sy is the major method for detecting cardiac transplant rejection; however, this approach is invasive

234 linically relevant disease states, including transplant rejection, hypertension, acute renal injury,

235 d and Drug Administration for prophylaxis of transplant rejection in 2011.

236 been used successfully for the treatment of transplant rejection in clinical practice, it may be a u

237 eration, abnormal growth, or immune mediated transplant rejection in either patient during the first

238 he strength, phenotype, or kinetics of heart transplant rejection in mice and (b) does not impact the

239 ed the rapidity of cardiac allograft or skin transplant rejection in mice.

240 has now been generated and is effective for transplant rejection in nonhuman primates and other mode

241 CTLA4Ig failed to block transplant rejection in primed mice, indicating that mem

242 reductions were found in risk of acute renal transplant rejection in recipients who possessed the CCR

243 ligand (aCD40L) can prevent autoimmunity and transplant rejection in several animal models and is cur

244 tagonists, such as CTLA4Ig, which suppresses transplant rejection in small animal models.

245 This response contributes to transplant rejection in that its modulation affects card

246 may actually be potent facilitators of organ transplant rejection in the absence of T-bet and RORgamm

247 onfer susceptibility to multiple acute liver transplant rejections in the German population.

248 es are a major factor in producing "chronic" transplant rejection, including the arteriopathy (athero

249 induce graft beds that promote high risk of transplant rejection, intrastromal corneal sutures were

250 d during this study suggest that small bowel transplant rejection is associated with changes in the m

251 Early transplant rejection is associated with increased MUC2,

252 Heart transplant rejection is characterized pathologically by

253 f their role in transplant immunobiology and transplant rejection is extremely limited and fragmentar

254 Organ transplant rejection is mediated largely by circulating

255 Transplant rejection is mediated primarily by adaptive i

256 oth in the pathogenesis of infections and in transplant rejection is now being explored.

257 of immune response to tissue-specific Ags in transplant rejection is poorly defined.

258 receptor CXCR4 in human kidney and in renal transplant rejection is unknown.

259 which is by itself ineffective in prolonging transplant rejection, is much more efficacious in prolon

260 In response to a second hepatocyte transplant, rejection kinetics were enhanced in both CD4

261 nt are major determinants of the kinetics of transplant rejection, little is known about the contribu

262 on regimens that have reduced rates of acute transplant rejection, long-term allograft survival remai

263 CD4+ T cells, essential for transplant rejection, may mediate ischemic ARF.

264 ce of C1q and other complement components in transplant rejection mechanisms.

265 During transplant rejection, migrating T cells infiltrate the g

266 71 is efficacious in a rat heterotopic heart transplant rejection model.

267 seases as diverse as lymphedema, filariasis, transplant rejection, obesity, and tumor metastasis.

268 Acute transplant rejection occurred more frequently in grafts

269 ferences were sufficient to stimulate robust transplant rejection of wild-type cells in mutant mice.

270 o protect the host and chronic inflammation, transplant rejection, or other disorders may occur.

271 ional relevance of the semidirect pathway to transplant rejection, our findings provide a solution to

272 This suggests that a capacity to regulate transplant rejection pre-exists in naive mice, and may b

273 ofetil is well tolerated and has lower renal transplant rejection rates than azathioprine regimens.

274 n B cells, yet its role in antibody-mediated transplant rejection remains unclear.

275 thritis (RA) and prevention of chronic organ transplant rejection, respectively.

276 , patients with myocarditis had similar post-transplant rejection, retransplantation, and survival ra

277 n used safely and effectively to treat renal transplant rejection since 1999.

278 they may represent the natural initiators of transplant rejection, spontaneous tumor rejection, and s

279 l models of autoimmune disease and allograft transplant rejection, suggesting their potential as nove

280 Indications for EMB included heart transplant rejection surveillance (846) and the evaluati

281 of CD4(+) T cells, mediate cytotoxicity and transplant rejection that is exclusively TNF-alpha/TNFR-

282 ases, including vascular disease and chronic transplant rejection, that involve vascular endothelial

283 sporine (CsA), the current mainstay of organ transplant rejection therapy.

284 torically, antibodies were thought to elicit transplant rejection through complement mediated damage

285 number of T cells that typically drive acute transplant rejection through their ability to directly i

286 se, with important implications ranging from transplant rejection to tumor immunotherapies.

287 h NK cells in a model of Tcell-mediated skin transplant rejection under costimulatory blockade condit

288 development to treat autoimmune diseases and transplant rejection, underscoring the importance in und

289 hypothesize that CO may protect against lung transplant rejection via its anti-inflammatory and antia

290 Autoreactivity can develop after transplant rejection via the indirect pathway.

291 Transplant rejection was compared in two inbred strains

292 vel therapeutic targets for autoimmunity and transplant rejection, we developed and performed a large

293 ys in identifying pathways involved in organ transplant rejection, we examined the gene expression pr

294 of regulatory T cells capable of preventing transplant rejection, we have developed two different st

295 The rates of corneal transplant rejection were similar among B-cell-deficient

296 haptoglobin enhanced the onset of acute skin transplant rejection, whereas haptoglobin-deficient skin

297 lant recipients and those experiencing acute transplant rejection, which revealed hundreds of differe

298 l. debunk two classical paradigms concerning transplant rejection, with important consequences for th

299 ing skin necrosis contributes to accelerated transplant rejection, with potential implications for th

300 variety of corneal abnormalities, including transplant rejection, wound healing and microbial kerati