ライフサイエンスコーパス: alloreactivity

1 donor-vs-recipient natural killer [NK]-cell alloreactivity).

2 vere inflammation and delayed the subsequent alloreactivity.

3 SCT and could represent a target to modulate alloreactivity.

4 ity assays were performed to evaluate T-cell alloreactivity.

5 al trials demonstrate that nTreg can control alloreactivity.

6 generated cells exhibited significant lower alloreactivity.

7 kine receptor CCR5 appears to play a role in alloreactivity.

8 e evidence that aging enhances CD8(+) T cell alloreactivity.

9 th allogeneic MHC, is the primary limiter on alloreactivity.

10 , even in the absence of detectable indirect alloreactivity.

11 MHC molecules, is the primary determinant of alloreactivity.

12 n and thereby favors the indirect pathway of alloreactivity.

13 D target tissues without abolishing antihost alloreactivity.

14 body has renewed our interest in subclinical alloreactivity.

15 both capable of inducing direct CD4+ T-cell alloreactivity.

16 hy associated with enhanced recipient T-cell alloreactivity.

17 perative transplant period may modulate host alloreactivity.

18 ajor feature of the TCR repertoire is strong alloreactivity.

19 ) proteins in an enigmatic phenomenon termed alloreactivity.

20 r contributing to graft rejection along with alloreactivity.

21 ndependent association between TTV level and alloreactivity.

22 ients, we performed several assays to assess alloreactivity.

23 the specific involvement of self-peptides in alloreactivity.

24 the skin, whereas imiquimod augmented their alloreactivity.

25 T and greatly reduced donor anti-host T cell alloreactivity.

26 ogen-specificity and evidence of nonspecific alloreactivity.

27 ell population to suppress CD4 cell-mediated alloreactivity.

28 ndings in the context of TCR restriction and alloreactivity.

29 cell repertoire exhibits a high frequency of alloreactivity.

30 igen-negative cells are markedly depleted of alloreactivity.

31 consistently attained (90%-95%) depletion of alloreactivity.

32 ponsible for a major part of the observed NK alloreactivity.

33 interactions between CMV and the recipient's alloreactivity.

34 fts that experience the added insult of host alloreactivity.

35 nagement requires understanding the basis of alloreactivity.

36 antigens in Dark Agouti (DA) rats modulates alloreactivity.

37 ing less IgG and IgM RBC xenoreactivity than alloreactivity.

38 n in vivo graft-versus-host disease model of alloreactivity.

39 antigen presentation to T cells and abolish alloreactivity.

40 ersensitivity (DTH) were used as measures of alloreactivity.

41 y of high-dose cyclophosphamide to eliminate alloreactivity.

42 ns in the regulation of donor-anti-recipient alloreactivity.

43 d mice showed limited capacities to generate alloreactivity.

44 or cells or a third party to assess relative alloreactivity.

45 y explain both self MHC restriction and high alloreactivity.

46 me was related to serum IgG anti-HLA class I alloreactivity.

47 molecular pathways that regulate pathogenic alloreactivity.

48 ved tumor-induced Mphi suppression of T cell alloreactivity.

49 llogenic) MHC molecules, a phenomenon called alloreactivity.

50 t such effects decrease rather than increase alloreactivity.

51 ibiting GVHD while preserving GVL effects of alloreactivity.

52 y a pivotal immunosuppressive role in T cell alloreactivity.

53 or longevity of the response at the price of alloreactivity.

54 nds partly on donor natural killer (NK) cell alloreactivity.

55 AC6-specific inhibitor (KA1010) in models of alloreactivity.

56 nsplant setting and its impact on anti-graft alloreactivity.

57 rved, likely by augmenting underlying T-cell alloreactivity.

58 possible role of iTreg in the regulation of alloreactivity.

59 e CD8 T-cell clone, confirming no semidirect alloreactivity.

60 lay a role in CD28/CTLA-4 blockade-resistant alloreactivity.

61 is associated with a lack of indirect T cell alloreactivity.

62 tent and selective approach to inhibition of alloreactivity.

63 on in vivo while inhibiting IFN-gamma driven alloreactivity.

64 etween patients with or without predicted NK alloreactivity (42% vs 52% at 1 year, P = NS).

65 Patients with acute biopsy-proven alloreactivity according to the Banff classification (n

66 Notch was found to be a central regulator of alloreactivity across clinically relevant models of tran

67 The influence of sex on alloreactivity, acute rejection, transplant-related coro

68 ed donor Th9 cells would augment or restrict alloreactivity after experimental bone marrow transplant

69 improve immune reconstitution while limiting alloreactivity after HLA-mismatched hematopoietic stem c

70 ansplantation than in patients who showed no alloreactivity after the first 6 mo after transplantatio

71 Alloreactivity after transplantation is associated with

72 alloresponses but failed to develop indirect alloreactivity after transplantation.

73 ord blood KIR3DL1 NK cells exhibited a basal alloreactivity against Bw4 target cells that increased u

74 CD8(+) T suppressor cells that inhibited Th alloreactivity against graft HLA antigens.

75 Expanded lymphocytes lack alloreactivity against recipient and other allogeneic ce

76 nd likely promotes damaging autoimmunity and alloreactivity against transplanted islets.

77 Alloreactivity against unrelated third-party cells was p

78 inically useful method of measuring indirect alloreactivity among human renal transplant recipients w

79 ionale for the prospective study of indirect alloreactivity among transplant recipients, to allow pre

80 tailor immunosuppressive drugs might prevent alloreactivity and adverse effects simultaneously.

81 In DOCK2-deficient mice, alloreactivity and allocytotoxicity were suppressed sign

82 d, focusing on structural data pertaining to alloreactivity and auto-reactivity and discuss implicati

83 ests important mechanistic variances between alloreactivity and autoimmunity in terms islet graft los

84 Our analysis suggests that alloreactivity and average self MHC restriction both can

85 We investigated alloreactivity and chimerism in a highly sensitized 40-y

86 -/-)) allogeneic Tconv, which possess normal alloreactivity and cytotoxicity, induce significantly le

87 endogenous TCR and HLA genes, which removes alloreactivity and decreases immunogenicity of third-par

88 historical development of assays to measure alloreactivity and discuss how high-throughput T cell re

89 Understanding the determinants of NK cell alloreactivity and function will support improvements in

90 The influence of sex on alloreactivity and graft outcome after heart transplanta

91 In contrast, PKCtheta was required for alloreactivity and GVHD induction.

92 onuclear cells (PBMCs), which showed minimal alloreactivity and high levels of HLA tetramer binding,

93 eceptor blockade is effective for preventing alloreactivity and high-grade rejection in cardiac trans

94 monitoring posttransplant changes in T cell alloreactivity and immunosuppression.

95 ested the hypothesis that ubiquitin inhibits alloreactivity and increases allograft survival in a mur

96 TI is required in this model to overcome alloreactivity and possibly to make "space" in the recip

97 ications for the mechanisms and frequency of alloreactivity and promiscuity in T cell responses.

98 ying administration effectively inhibits the alloreactivity and promotes the dominance of intragraft

99 proliferation of TEM cells and their ex vivo alloreactivity and resulted in their significant reducti

100 iac transplantation, reducing serum anti-HLA alloreactivity and shortening the duration to transplant

101 immunity by reducing graft-vs-host directed alloreactivity and the associated elimination of the rec

102 e involved; however, the molecular basis for alloreactivity and the contribution of self-peptides are

103 al CD4(+) T(reg) are critical in controlling alloreactivity and the establishment of tolerance.

104 Here we review the determinants of NK cell alloreactivity and their implications for adoptive NK ce

105 ceptor sequestration model in the context of alloreactivity and transplantation.

106 The effects of these regimens on anti-HLA alloreactivity and waiting time to transplantation were

107 chanisms would result in a better control of alloreactivity and would represent a regulatory T-cell-c

108 ce showed increased frequency of CD8+ T cell alloreactivity and, interestingly, expansion of virus-in

109 type splenocytes in proliferation responses, alloreactivity, and expression of cell surface markers i

110 vivo transduction, expansion, maintenance of alloreactivity, and ganciclovir-mediated ablation of can

111 and effects, suggests a structural basis for alloreactivity, and illustrates how bacterial superantig

112 cts of anti-CD154 treatment on autoimmunity, alloreactivity, and inflammatory events mediated by macr

113 cts of anti-CD154 treatment on autoimmunity, alloreactivity, and proinflammatory events mediated by m

114 the impact of the alarmin interleukin-33 on alloreactivity, and the role of Notch ligands expressed

115 Alloreactivity appeared to contribute to the in vitro an

116 curtails self specificity without affecting alloreactivity are discussed.

117 sensitization and effector phases of humoral alloreactivity as well as efficacy testing of future imm

118 ic splenocytes in vivo resulted in increased alloreactivity, as determined by IFNgamma production.

119 layed protocol significantly inhibited donor alloreactivity at d30 as compared to the early protocol.

120 he failure of Mer-deficient hosts to provoke alloreactivity, because Mer(-/-) spleen cells were recog

121 Patients with high alloreactivity but low anti-GalT-KO xenoreactivity were

122 dose (3 g/kg) IVIg was effective in reducing alloreactivity but was associated with a high incidence

123 antileukemic functionality in the absence of alloreactivity, but long-term persistence in vivo is bet

124 of Th1 differentiation was shown in indirect alloreactivity, but this suppression could also be media

125 erleukin-2 yielded lymphocyte clones without alloreactivity, but with strong proliferative responsive

126 s that in patients with cGVHD, ECP modulates alloreactivity by affecting activated lymphocyte populat

127 Our results suggest that ECP alters alloreactivity by affecting allo-targeted effector T cel

128 e able to delay graft rejection after direct alloreactivity by controlling proliferation and differen

129 lls have made it difficult to study indirect alloreactivity by using currently available assays.

130 Tolerance induction and alloreactivity can be applied to the clinic for the tran

131 rscored by the growing body of evidence that alloreactivity can be profoundly influenced by infection

132 These findings confirm that NK alloreactivity can occur in HLA-matched HSCT, where tole

133 However, paradoxically, alloreactivity can proceed with high peptide and MHC spe

134 ors able to exert donor-vs-recipient NK-cell alloreactivity carry KIR2DS1 and/or KIR3DS1, searching f

135 etermining in vitro proliferation responses, alloreactivity, cell surface marker expression, and anti

136 tation, these cells did not exhibit enhanced alloreactivity compared with young memory T cells.

137 that in the absence of Th1 immunity, CD8 T17 alloreactivity constitutes a barrier to transplantation

138 determine if "classical" in vitro assays of alloreactivity could also detect linked suppression and

139 Such direct alloreactivity could be detected for more than 1 y after

140 d in a family, the prediction of KIR NK cell alloreactivity could be of crucial importance for donor

141 Antihost alloreactivity could be reactivated in stable graft-vers

142 nificantly suppressed capacity to induce MHC alloreactivity, CTL responses, and IL-12 production.

143 The risk for alloreactivity decreased by 10% per log level of TTV cop

144 matched molecules, the probability of T cell alloreactivity decreases.

145 ges of transplantation is the development of alloreactivity despite the use of multiagent immunoproph

146 Natural killer (NK)-cell alloreactivity, determined by donor killer-cell immunogl

147 ts were PRA+/PRT-75+, indicating that T cell alloreactivity did not routinely imply B cell sensitizat

148 In the absence of donor-vs-recipient NK-cell alloreactivity, donor activating KIRs had no effects on

149 Intact alloreactivity-driven antitumor cytokine responses resul

150 fluence of solid tumors on the occurrence of alloreactivity-driven GvHD and graft-versus-solid tumor

151 the strategies directed primarily at T-cell alloreactivity enhanced engraftment in sensitized mice.

152 Despite uninhibited alloreactivity, exogenous IL-22 administration posttrans

153 identifying a dual TCR T cell with distinct alloreactivities for each TCR.

154 rnatants do not differentiate primary T-cell alloreactivity from recall responses in allograft-primed

155 NK cell alloreactivity has been defined by the absence of recipi

156 Because pretransplant T-cell alloreactivity has been shown to increase the risk of po

157 The beneficial clinical effect of NK-cell alloreactivity has not been uniformly demonstrated, like

158 In an in vitro model of alloreactivity, human lymphoma B cells with TNFRSF14 abe

159 ible that there will be a benefit of NK cell alloreactivity if strategies of haploidentical transplan

160 Limitations on alloreactivity imposed by a requirement for recognition

161 The remaining T cells had negligible alloreactivity in a secondary MLR.

162 ery amino acid difference will affect T cell alloreactivity in a similar way; we hypothesized that th

163 ually serve as a disease biomarker of T-cell alloreactivity in aGVHD.

164 sents an opportunity to efficiently modulate alloreactivity in allo-HCT to either exacerbate it for a

165 how high specificity for EBV with negligible alloreactivity in both proliferation and cytotoxicity as

166 (IL)-2 receptor effectively prevented T-cell alloreactivity in cardiac transplantation.

167 e endogenous TCR in T cells strongly ablated alloreactivity in comparison with TCR-expressing T cells

168 he CD8(+)TCR- population demonstrated strong alloreactivity in culture.

169 ith ITx and can likely substitute for T-cell alloreactivity in estimating rejection risk in this rare

170 Earlier diagnosis and management of alloreactivity in female recipients before development o

171 ts to manipulate TCR recognition, as well as alloreactivity in general.

172 Donor natural killer (NK) cell alloreactivity in HCT can control leukemic relapse, but

173 actions allow predicting natural killer cell alloreactivity in hematopoietic stem cell transplantatio

174 can control leukemic relapse, but capturing alloreactivity in HLA-matched HCT has been elusive.

175 ter understanding of the T cells involved in alloreactivity in humans, we developed a cytokine flow c

176 r risk stratification of acute biopsy-proven alloreactivity in kidney transplant recipients and might

177 Twenty-four-hour analysis of alloreactivity in mice that rejected fully MHC-disparate

178 the potential benefits of exploiting NK cell alloreactivity in mismatched hematopoietic stem cell tra

179 id organs in vivo and despite their in vitro alloreactivity in mixed leukocyte reaction (MLR) assays

180 To better characterize alloreactivity in naive and skin allograft-primed mice,

181 could play a role in infection clearance or alloreactivity in patients with acute leukaemia who rece

182 moral immunity as playing a dominant role in alloreactivity in sensitized recipients.

183 tested for correlations with donor-specific alloreactivity in simultaneous mixed lymphocyte co-cultu

184 uthors discuss myeloid self-antigen-directed alloreactivity in the context of our evolving understand

185 time, the significant impact of KIR NK cell alloreactivity in the determination of which UCB unit wi

186 The development of alloreactivity in the host was confirmed by mixed lympho

187 upon PT-Cy administration, blunting NK cell alloreactivity in this transplantation setting.

188 l be followed to evaluate and manage humoral alloreactivity in VCA recipients.

189 nhibitory activity of soluble ILT3 on T cell alloreactivity in vitro and in vivo suggests the potenti

190 g) cells have been implicated in suppressing alloreactivity in vitro and in vivo.

191 e antigen-specific and showed no nonspecific alloreactivity in vitro and in vivo.

192 is absent on leukemic target cells can exert alloreactivity in vitro and in vivo.

193 49s3-expressing NK cells drastically reduced alloreactivity in vitro, indicating that this subpopulat

194 ntigen-1 (LFA-1) interaction in human T cell alloreactivity in vitro.

195 Therefore, these data indicate that NK cell alloreactivity in vivo is dependent on the combination o

196 ce process dynamically modulates the NK cell alloreactivity in vivo.

197 so endowed with the capacity to downregulate alloreactivity inducing tolerogenic responses.

198 Thymic positive selection and the mode of alloreactivity induction are the major independent facto

199 nt pairs may correlate with the magnitude of alloreactivity influencing the development of DGF.

200 Direct T-cell alloreactivity involves recognition of the allogeneic mo

201 rism correlated negatively with DLI-mediated alloreactivity irrespective of the timing of their admin

202 This ratio is at best 5 if alloreactivity is 5%.

203 her complete elimination of all rejection or alloreactivity is a desirable goal in liver transplantat

204 Natural killer (NK) cell alloreactivity is favored after double umbilical cord bl

205 affects natural killer (NK) cells and their alloreactivity is largely unknown.

206 In view of the growing evidence that alloreactivity is mainly derived from human naive T cell

207 Deeper knowledge of NK-mediated alloreactivity is necessary to predict its contribution

208 Given that alloreactivity is predominantly a cross-reactive phenome

209 rsus-host disease (GVHD), but whether direct alloreactivity is sufficient for the propagation of GVHD

210 Alloreactivity is the response of T cells to MHC molecul

211 higher in patients who displayed persistent alloreactivity late after transplantation than in patien

212 that intragraft nTreg are unable to restrain alloreactivity leading to rejection.

213 We also find that the alloreactivity level can be inferred directly from data

214 t macrophages, although unlikely to initiate alloreactivity, may contribute to GVHD by sustaining the

215 Donor-specific alloreactivity measured with CD154(+) T-cytotoxic memory

216 We hypothesize, that NK cell alloreactivity mediated by killer cell immunoglobulin-li

217 erentially inhibited cytokine production and alloreactivity mediated by naive and central memory huma

218 ells are excluded to limit the potential for alloreactivity mediated by native TCR coexpressed by HA-

219 Functional analysis showed that the alloreactivity mediated by these infiltrating MIP-3alpha

220 lts suggest that serial immune monitoring of alloreactivity might be beneficial when immunizations ar

221 It has been proposed that alloreactivity occurs because self and foreign MHCs bind

222 In HLA-mismatched HSCT, alloreactivity occurs when licensed donor NK cells expre

223 and activation are affinity-driven, then an alloreactivity of 1-24% is incompatible with the textboo

224 We examined the I-Ep alloreactivity of a well-characterized Hb(64-76)/I-Ek-sp

225 .006) and inversely correlated with enhanced alloreactivity of CD154+ T-cytotoxic memory cells (r=-0.

226 therapy with T-regulatory cells controls the alloreactivity of conventional T lymphocytes in animal m

227 eactivated memory cells were reduced and the alloreactivity of DCs was diminished.

228 Alloreactivity of donor lymphocytes leads to graft-versu

229 aft-versus-host disease (GVHD) is induced by alloreactivity of donor T cells toward host antigens pre

230 m tumor immunization of donors, the in vitro alloreactivity of immune recipients was more restricted

231 Alloreactivity of KIR2DL1(+) NK cell subsets against C1C

232 ession by miR-181a may contribute to altered alloreactivity of T cells in aGvHD.

233 ve demonstrated the clinical benefit of such alloreactivity of the donor-derived NK cell system in pa

234 In this study, we examined the alloreactivity of the innate NK cells in Rag(-/-) mice u

235 ype morphology in lymph nodes, and increased alloreactivity of third-party responders to peripheral b

236 We investigated the impact of KIR NK cell alloreactivities on the dominance of 1 full UCB unit in

237 The presence of alloreactivity on day 100 was confirmed in vivo by adopt

238 erism influences the potency of DLI-mediated alloreactivity only in the MHC-mismatched but not MHC-ma

239 T cells with unwanted specificities such as alloreactivity or autoreactivity are a consequence of si

240 eration by heterogeneous Tregs is not due to alloreactivity or crossreactivity.

241 , similar results were found in the indirect alloreactivity pathway only when nTregs were used in hig

242 Human T-cell alloreactivity plays an important role in many disease p

243 plantation, despite potential donor antihost alloreactivity present in most transplants.

244 Natural killer cell alloreactivity reduces graft-versus-host disease while a

245 plantation; however, the molecular basis for alloreactivity remains elusive.

246 C-matched chimeras, the induction of optimal alloreactivity requires not only donor T cells and host

247 his approach, we determined that most T-cell alloreactivity resided within the CD4(+) T-cell subset,

248 Thus, infections can result in enhanced alloreactivity, resistance to tolerance induction, and d

249 isplayed a polyclonal repertoire in terms of alloreactivity, responses to foreign protein antigens, a

250 s tested and was largely responsible for the alloreactivity resulting from tumor immunization of dono

251 een in patients with SJS/TEN, as well as the alloreactivity seen in patients with GVHD.

252 This unique alteration in host alloreactivity, seen not only in peripheral lymphocytes

253 nt for the experimentally observed levels of alloreactivity, self MHC restriction and the frequency o

254 Analysis of alloreactivity showed that CD18-/- and WT T cells had co

255 Gcnt1-deficient T cells still drove lethal alloreactivity, showing that core-2 O-glycosylation pred

256 and LFA-1 resulted in profound inhibition of alloreactivity, suggesting that combined anti-CD154/anti

257 opoietic cell transplantation (HCT) if donor alloreactivity targets the recipient.

258 Using an established alloreactivity TCR transgenic model, blockade of TIM-3 i

259 ost LCLs more consistently depleted in vitro alloreactivity than stimulation with host PBMCs, as asse

260 lts demonstrate the complex character of the alloreactivity that develops during ongoing immunoprophy

261 intage may also explain the increased T cell alloreactivity that previously was observed in black kid

262 ematical expressions giving the frequency of alloreactivity, the level of self-MHC restriction, and t

263 gous and allogeneic tumors and are devoid of alloreactivity, these results provide preclinical proof

264 tion may provide a strategy to decrease host alloreactivity through the production of a chimeric stat

265 and IFN-gamma reduces the potential of this alloreactivity to cause epithelial tissue GVHD.

266 t spot assay can be used to monitor indirect alloreactivity to donor HLA-DR peptides among renal tran

267 array assays allows characterization of host alloreactivity to individual HLA antigens with sufficien

268 plasmapheresis caused a similar reduction in alloreactivity to IVIg, this effect was achieved after l

269 DC marker; low phagocytic activity; and high alloreactivity to naive T cells.

270 herapeutic natural killer (NK)-cell-mediated alloreactivity toward acute myeloid leukemia has largely

271 e three TCRs exhibited differing patterns of alloreactivity toward closely related or distinct HLA-I

272 ion model that NK cells mediate considerable alloreactivity toward pediatric BCP-ALL in vivo.

273 splant pairs with donor-vs-recipient NK-cell alloreactivity, transplantation from donors with KIR2DS1

274 ack of MyD88 signaling in donor Tcons during alloreactivity uses the ST2 but not the IL-1R or TLR4 pa

275 The ultimate outcome of alloreactivity versus tolerance following transplantatio

276 tor-responder pairs, the median reduction of alloreactivity was 474-fold (range, 43-fold to 864-fold)

277 A similar lack of indirect alloreactivity was also observed after placement of diff

278 Antihost alloreactivity was associated with reduction of posttran

279 s stimulators, a 100-fold (99%) reduction in alloreactivity was attained, resulting in abrogation of

280 Although both were efficiently taken up, alloreactivity was limited to the semi-direct pathway, a

281 Suppression of donor-anti-recipient alloreactivity was not observed in mixed lymphocyte co-c

282 However, loss of posttransplant alloreactivity was observed at 3 weeks.

283 Additionally, alloreactivity was observed between the genetically drif

284 ion experiments, we further showed that this alloreactivity was restricted to the class II molecule I

285 The potency of Th9 cell inhibition of alloreactivity was similar to that of rapamycin resistan

286 lpha inhibition on dendritic cell-stimulated alloreactivity, we demonstrate here that JAK2 represents

287 ossible mechanism by which IL-17 may promote alloreactivity, we examined the influence of IL-17 on th

288 e corresponding phenotype and donor-specific alloreactivity were characterized in peripheral blood.

289 ocytes from these tolerant mice have reduced alloreactivity when restimulated in vitro.

290 eir physicochemical properties affect T cell alloreactivity, whereas in the alpha helices, both compa

291 enge of transplantation: lifelong control of alloreactivity while maintaining an otherwise intact imm

292 llografts might constitute a way of reducing alloreactivity while maintaining memory T-cell responsiv

293 major goal in transplantation is to prevent alloreactivity while preserving activity against tumors

294 This method reduces alloreactivity while retaining reactivity against third-

295 of a single T-cell manipulation to eliminate alloreactivity while sparing antiviral and antitumor T c

296 sgenic (TCR-tg) mouse models with direct CD4 alloreactivity will help elucidate mechanisms of transpl

297 Abrogation of alloreactivity will lead to disease relapse, whereas unt

298 rmissive mismatches mediating limited T-cell alloreactivity with minimal toxicity, and describes futu

299 Reconciling the high frequency of alloreactivity with the fact that only 1 T cell in 10(4)

300 a mean reduction of 33% in anti-HLA class I alloreactivity within 1 week.