ライフサイエンスコーパス: chimerism

1 ficant whole-blood chimerism, lacking T cell chimerism).

2 ing an individual with genome-wide suspected chimerism.

3 biotic gene transfer would lead to inherited chimerism.

4 nts and was associated with higher donor CD3 chimerism.

5 late development, thus limiting the cost of chimerism.

6 details on CMV infection episodes and T-cell chimerism.

7 s by induction of stable hematopoietic mixed chimerism.

8 al-transplant recipients with haematopoietic chimerism.

9 be achieved after the establishment of mixed chimerism.

10 te immunocompetence, and no peripheral blood chimerism.

11 or recipient-specific HLA marker to analyze chimerism.

12 including tolerance induction through mixed chimerism.

13 approach for attaining stable hematopoietic chimerism.

14 cing transplantation tolerance through mixed chimerism.

15 sents an obstacle to successful induction of chimerism.

16 was successful in all patients with durable chimerism.

17 e significantly expanded the clinical use of chimerism.

18 All dogs achieved stable mixed chimerism.

19 ent to 100 cGy for establishing stable mixed chimerism.

20 ismatched donors to induce mixed or complete chimerism.

21 1 year after transplantation had 100% donor chimerism.

22 ation between large antigenic skin loads and chimerism.

23 antilymphoma activity and promoted complete chimerism.

24 The remainder had stable mixed chimerism.

25 All seven patients achieved mixed chimerism.

26 likely to ensure sustained high-level donor chimerism.

27 ong-term hematopoietic engraftment and donor chimerism.

28 sis (HLH) at the cost of more frequent mixed chimerism.

29 s were exploited to quantify donor/recipient chimerism.

30 phar1(-/-)), had significantly reduced donor chimerism.

31 l transplants to establish mixed or complete chimerism.

32 onor-specific tolerance and mixed allogeneic chimerism.

33 tudies looking at long-term lineage-specific chimerism.

34 hieving excellent survival with high myeloid chimerism.

35 ncarrier donors and achieving complete donor chimerism.

36 ll chimerism and low B-cell and myeloid cell chimerism (0% to 46%).

37 en dogs had long-term donor mononuclear cell chimerism (19%-58%), whereas 1 dog treated with the lowe

38 ll treated animals revealed peripheral blood chimerism (4 weeks), most pronounced after repetitive ce

39 (155 muCi/kg) had low donor mononuclear cell chimerism (5%).

40 posttransplantation cyclophosphamide after a chimerism-ablating secondary recipient lymphocyte infusi

41 either mixed hematopoietic or CD8(+) T cell chimerism, above which immune regulation was reestablish

42 The levels of donor cell chimerism achieved in this study would be therapeutic fo

43 induce tolerance through mixed hematopoietic chimerism across a pig-to-primate barrier.

44 afts from all mice and benefit from enhanced chimerism after BCNU with less cell infiltrate and no ch

45 it in normal bone marrow cells and increases chimerism after bone marrow transplantation, indicating

46 Finally, conversion to donor chimerism after donor lymphocytes is associated with cli

47 We prospectively studied the kinetics of LC-chimerism after sex-mismatched allogeneic hematopoietic

48 and may explain why WAS patients with mixed chimerism after stem cell transplantation often develop

49 stem cell function, as evidenced by reduced chimerism after transplantation that was not rescued by

50 or unrelated donor recipients had full donor chimerism, all 3 recipients of mismatched unrelated dono

51 curred in 9 patients, and 2 had stable mixed chimerism; all patients had sustained correction of neut

52 Chimerism analysis of isolated CMV tet(low) and tet(high

53 itor transplant and HIV infection, including chimerism analysis, CCR5 genotyping and viral tropism, v

54 e resulted in a limited degree of donor cell chimerism and a differentiation program skewed toward my

55 ement that there was a higher rate of B-cell chimerism and a lower number of patients who required on

56 ts maintained mixed donor-host hematopoietic chimerism and accepted vascularized composite allografts

57 Cell-based therapies to facilitate chimerism and achieve tolerance in major histocompatibil

58 ) cells promotes durable mixed hematopoietic chimerism and allograft tolerance in mice receiving allo

59 recipients have better B-lymphocyte/myeloid chimerism and are free from immunoglobulin replacement t

60 ndent on the previous establishment of mixed chimerism and can be induced coincident with hematopoiet

61 ls required to achieve durable hematopoietic chimerism and donor-specific skin allograft tolerance an

62 ies of the fetus to achieve mixed allogeneic chimerism and donor-specific tolerance (DST).

63 We sought to analyze long-term chimerism and event-free survival in children undergoing

64 ts for maintenance of minimal posttransplant chimerism and for therapeutic strategies involving gene

65 ic MF CD34+ cells achieved a higher level of chimerism and generated both myeloid and lymphoid cells

66 For most of these targeted clones, chimerism and germline transmission can be scored throug

67 Mixed chimerism and graft-versus-host-disease (GVHD) remain li

68 Twelve have achieved stable donor chimerism and have been successfully taken off immunosup

69 We previously showed full donor chimerism and immunosuppression withdrawal in highly mis

70 rmediate hPSC type exhibits higher degree of chimerism and is able to generate differentiated progeni

71 d donor HSCT had high levels of donor T-cell chimerism and low B-cell and myeloid cell chimerism (0%

72 Chimerism and mixoploidy are defined by the presence of

73 ines during development is a likely cause of chimerism and mixoploidy in mammals.

74 ollowing IUHCT can be enhanced to high-level chimerism and near complete Hb replacement with normal d

75 ssion medication with continued stable donor chimerism and no graft-vs-host disease.

76 of either CD8(+) DCs or NKT cells abrogated chimerism and organ graft acceptance.

77 ed expression of Hmga2 resulted in increased chimerism and platelet counts in recipients of retrovira

78 chimerism compared with models of postnatal chimerism and provides additional support for the prenat

79 8 blockade induces multi-lineage, full donor chimerism and recipient-specific tolerance while maintai

80 Correlation between chimerism and rejection, graft failure, and patient surv

81 mphocytes and was sufficient to induce mixed chimerism and robust systemic tolerance across full majo

82 d and high levels of multilineage allogeneic chimerism and robust tolerance to the donor.

83 mmune response associated with conversion of chimerism and severe GVHD.

84 in the AfuTmV-1 genome is a striking case of chimerism and the first example (to our knowledge) of su

85 2V617F(+) Moreover, the degree of human cell chimerism and the proportion of malignant donor cells we

86 elapse incidence when administered for mixed chimerism and their utility as salvage therapy when give

87 d a new therapeutic approach to induce mixed chimerism and tolerance by a direct pharmacological modu

88 d ATG promoted the development of persistent chimerism and tolerance in a cohort of patients given ki

89 Unexpectedly, chimerism and tolerance were established in old recipien

90 relevant methods for inducing hematopoietic chimerism and transplantation tolerance, with a special

91 y be complicated by the development of mixed chimerism and uncertainty regarding the risk of HLH recu

92 Barcoded HSCs showed robust (>80% human chimerism) and reproducible myeloid and lymphoid engraft

93 version of mixed chimerism toward full donor chimerism, and a potentially favorable balance between G

94 w risk of acute GVHD, a higher risk of mixed chimerism, and delayed early lymphocyte recovery and tha

95 D, achievement of at least 90% myeloid donor chimerism, and incidence of graft failure after at least

96 alemtuzumab levels impact acute GVHD, mixed chimerism, and lymphocyte recovery following RIC HCT wit

97 lant alemtuzumab levels on acute GVHD, mixed chimerism, and lymphocyte recovery.

98 egulatory T-cell induction, peripheral blood chimerism, and microchimerism in lymphatic organs were a

99 life, manifests as constitutional mosaicism, chimerism, and mixoploidy in live-born individuals.

100 es, longitudinal immunoreconstitution, donor chimerism, and quality of life (QoL) of IL2RG/JAK3 SCID

101 duced in nonhuman primates through the mixed chimerism approach, if specific modifications to overcom

102 t mice decreased the degree of donor-derived chimerism as well as the JAK2V617F allele burden, indica

103 9 patients treated at Stanford who had mixed chimerism-associated CLL relapse, 4 (44%) converted to f

104 ll animals revealed peripheral multi-lineage chimerism at four weeks (P < 0.01) independent of cell t

105 anscriptome data to determine host and donor chimerism at single-cell resolution from bone marrow mon

106 Blood cell monitoring included changes in chimerism, balance of T-cell subsets and responses to do

107 cells (BMCs) has been demonstrated in mixed chimerism-based tolerance induction protocols; however,

108 vestigated the impact of immunosenescence on chimerism-based tolerance induction.

109 By contrast, transient chimerism-based tolerance is devoid of GVHD risk and app

110 d leukemia (AML) who converted to full-donor chimerism but developed severe acute GVHD after prophyla

111 l as host Tregs did not affect hematopoietic chimerism but it led to rapid loss of skin allografts.

112 e more likely to achieve full donor lymphoid chimerism by day +14 after transplant.

113 showed a high degree of passenger leukocyte chimerism by immunohistochemistry and flow cytometry.

114 Here, we test the hypothesis that mixed chimerism can be intentionally reverted to host hematopo

115 We recently reported that durable chimerism can be safely established in mismatched kidney

116 autoreactive T cells, and induction of mixed chimerism can effectively reverse these defects.

117 r studies indicate that MHC-mismatched mixed chimerism can mediate thymic deletion of cross-reactive

118 Multilineage chimerism, clonal deletion, and lymphocyte subsets were

119 Thus, we conclude that endothelial chimerism combined with vascular sequestration of DSAs p

120 of allospecific tolerance in prenatal mixed chimerism compared with models of postnatal chimerism an

121 ent coverage uniformity and markedly reduced chimerism compared with products of liquid MDA reactions

122 t and resulted in significantly higher donor chimerism compared with recipients conditioned with TGF-

123 tients receiving donor lymphocytes for mixed chimerism converted to full donor status.

124 Hematopoietic recovery and chimerism, cumulative density of infections, nonrelapse

125 The minimum level of donor chimerism (DC) required to prevent HLH reactivation in h

126 Complete donor chimerism (DC) within the CD19, CD3, and CD33 cell linea

127 Two subjects with only transient chimerism demonstrated subclinical rejection on protocol

128 f CIs induced long-term germline and somatic chimerism, demonstrating self-renewal and pluripotency o

129 Therefore, induction of MHC-mismatched mixed chimerism depletes pre-existing and de novo-developed au

130 Subjects with persistent chimerism developed few serious infections when off IS.

131 HIV-1 correlated temporally with full donor chimerism, development of graft-versus-host disease, and

132 ype NOD mice, although induction of complete chimerism did prevent the disease.

133 patients experienced declining donor myeloid chimerism (DMC) levels with eventual return of disease.

134 Chimerism endows colonies with increased virulence and a

135 Mixed donor-host chimerism, established through hematopoietic cell transp

136 We next demonstrated that through chimerism, EWS-FLI acquired the ability to alter chromat

137 sorting analyses were performed for testing chimerism, expression of markers of activation and suppr

138 CLL relapse, 4 (44%) converted to full donor chimerism following ibrutinib initiation, in association

139 atal "boosting" strategy; and (3) high-level chimerism following IUHCT and postnatal "boosting" resul

140 he murine SCD and Thal models; (2) low-level chimerism following IUHCT can be enhanced to high-level

141 itor colonies and peripheral blood leukocyte chimerism following transplantation into conditioned hos

142 t-versus-host disease (GVHD), and eight with chimerism for at least 6 months were withdrawn from anti

143 Finally, we describe the kinetics of chimerism for several lymphocyte populations as well as

144 ier, namely thymus transplantation and mixed chimerism, from their inception in rodent models through

145 tissue components was placed in animals with chimerism greater than or equal to 1% on day 28.

146 ogeneic or (hostXdonor)F1-Tcm, support donor chimerism (> 6 months) in sublethally irradiated (5.5Gy)

147 complete donor chimerism or high-level mixed chimerism (>50% donor chimerism) in all lineages.

148 erity, time to engraftment, lineage-specific chimerism, immune reconstitution, and discontinuation of

149 infusion resulted in a significant change of chimerism in 1 of 3 male recipients without any signs of

150 clinically relevant levels of hematopoietic chimerism in a canine model of maternal-to-fetal IUHCT.

151 Treg cell BMT that were evaluable displayed chimerism in all lineages, including T cells, for up to

152 nsplant tolerance has been achieved by mixed chimerism in animal models and in a limited number of ki

153 Blood spot DNA from this subject displayed chimerism in CSF1R acquired after haematopoietic stem ce

154 d Dlk1-Dio3 gene cluster and fail to produce chimerism in mice.

155 ency and ability to contribute to high-grade chimerism in mice.

156 nt iPSCs and enables them to form high-grade chimerism in mice.

157 med into iPSCs that contribute to high-grade chimerism in mice.

158 permits establishment of mixed hematopoietic chimerism in mice.

159 nditioning plus FCRx safely achieved durable chimerism in mismatched allograft recipients.

160 social interaction, particularly by reducing chimerism in multicellular fruiting bodies that develop

161 The cumulative incidence of mixed chimerism in patients with an alemtuzumab level </=0.15

162 lls sustained significantly higher levels of chimerism in primary and secondary recipients than CD166

163 sults are the first to demonstrate prolonged chimerism in primates treated with CD28/mTOR blockade an

164 angerin-staining was used to assess donor LC-chimerism in skin biopsies obtained on days 28, 56, and

165 Allogeneic transplant led to donor-recipient chimerism in sperm from 2/6 adult recipients.

166 eightened levels of human hematopoietic cell chimerism in the absence of irradiation.

167 We used mixed hematopoietic chimerism in the canine model of major histocompatibilit

168 Conversion of chimerism in the presence of GVHD after CD4 donor lympho

169 The change in chimerism in the recipient occurred in association with

170 Examination of chimerism in the reconstituted B6.g7 mice showed that B

171 TBI dose capable of achieving complete donor chimerism in this mouse strain combination was 325 cGy g

172 Furthermore, induction of mixed chimerism in transgenic BDC2.5-NOD mice with MHC-matched

173 sm or high-level mixed chimerism (>50% donor chimerism) in all lineages.

174 end points were the level of donor leukocyte chimerism; incidence of acute and chronic graft-vs-host

175 in controls; both myeloid and lymphoid cell chimerism increased because of higher engraftment of HSC

176 tolerance, the mechanistic requirements for chimerism-induced tolerance are not clearly elucidated.

177 Mixed chimerism induces donor-specific tolerance to kidney and

178 ecule Bcl-2 inhibitor ABT-737 promoted mixed chimerism induction and reversed the antitolerogenic eff

179 ough there is evidence linking hematopoietic chimerism induction and solid organ transplant tolerance

180 istic underpinning for the susceptibility to chimerism induction despite increased TMEM frequencies.

181 us in a well-established primate bone marrow chimerism-induction model.

182 Sustained T-cell chimerism is a more robust biomarker of tolerance than d

183 splantation.Induction of mixed hematopoietic chimerism is a robust approach to establishing such tran

184 Mixed chimerism is an effective approach for tolerance inducti

185 ansplantation, in which tolerance and stable chimerism is induced after conditioning with fractionate

186 Hematopoietic chimerism is known to promote donor-specific organ allog

187 that in some settings, transient T cell-poor chimerism is not sufficient to induce tolerance to a con

188 lative HSC transplants (HSCTs), stable mixed chimerism is sufficient to reverse the disease.

189 ed donor chimerism, (significant whole-blood chimerism, lacking T cell chimerism).

190 Enhanced mixed chimerism leads to long-term donor-specific allograft to

191 High chimerism levels were induced across multiple hematopoie

192 Chimerism levels were significantly higher in treated pu

193 level was 48% (95% CI, 34%-62%); the myeloid chimerism levels, 86% (95% CI, 70%-100%).

194 ients ended up with very low levels of donor chimerism (<10% donor), especially in the myeloid lineag

195 tance had established higher levels of donor chimerism, lymphocyte responses which were attenuated to

196 Mixed chimerism may be clinically reverted to 100% recipient w

197 some cells, whether achieved by mosaicism or chimerism, may confer benefit in hereditary diffuse leuk

198 nt studies suggest that MHC-mismatched mixed chimerism mediates negative selection of autoreactive th

199 matched H-2(b) but not matched H-2(g7) mixed chimerism mediates thymic deletion of the cross-reactive

200 ere, we investigated in mice whether durable chimerism might be enhanced by pre-treatment of the reci

201 achieved using MGMT transgenic BM in a mixed-chimerism model receiving BCNU across a major histocompa

202 All patients, including those with mixed chimerism, mounted robust antibody responses to vaccinat

203 recipients with an average level of initial chimerism of 11.7% (range 3% to 39%) without conditionin

204 hereas heart macrophages showed a much lower chimerism of 2.7+/-0.5% (P<0.01).

205 After 6 weeks, we observed blood monocyte chimerism of 35.3+/-3.4%, whereas heart macrophages show

206 ce pluripotency, but did selectively enhance chimerism of MiP-derived tissue in both fetal and adult

207 ations show decreased peripheral and central chimerism of PHD2-deficient cells but not of the most pr

208 donor-derived erythrocytes and stable mixed chimerism of recipient-derived and donor-derived leucocy

209 oductive adaptations, including hematopoetic chimerism of siblings, suppression of reproduction in no

210 nd noncompetitive repopulation assays (<1.5% chimerism of Vav1(-/-) cells vs. 53-63% for wild-type ce

211 he impact of impermanent, T cell-poor, mixed-chimerism on renal allograft survival.

212 In a primitive chordate model of natural chimerism, one chimeric partner is often eliminated in a

213 all surviving patients, either stable mixed chimerism or full donor chimerism were observed.

214 than 90% of patients achieved complete donor chimerism or high-level mixed chimerism (>50% donor chim

215 either simultaneously to induction of mixed chimerism or into established mixed chimeras 85-150 days

216 w Transplantation guidelines without loss of chimerism or rejection.

217 re limited either by loss of long-term mixed chimerism or risk of graft-versus-host disease (GVHD).

218 The chimerism or the beneficial graft-versus-leukemia respon

219 rapy did not affect the degree of human cell chimerism or the proportion of malignant donor cells.

220 Full-donor chimerism (P = .039) and normal enzyme levels (P = .007)

221 esented a higher frequency of complete donor chimerism (P = .04) and faster total lymphocyte count re

222 enal allograft and that the presence of this chimerism per se is not an independent biomarker to iden

223 ansduced hCB cells as long as human platelet chimerism persisted.

224 ncrease after dUCBT, and early CD4(+) T-cell chimerism predicts for graft predominance.

225 After T-Rapa cell infusion, mixed donor/host chimerism rapidly converted, and there was preferential

226 eatment was associated with early failure of chimerism, regardless of Treg cell administration.

227 VA-specific CD4(+) and CD8(+) T cells led to chimerism rejection, which was inhibited by treatment wi

228 Donor cell chimerism remained stable for up to 2 years and was asso

229 es complexity modeled on a real counterpart, chimerism remained within the same species for most cont

230 Graft acceptance and chimerism required host CD4(+)CD25(+) Treg production of

231 report whether approaches resulting in mixed chimerism result in clinically relevant immune reconstit

232 Importantly, this chimerism resulted in successful donor skin acceptance,

233 Induction of MHC-mismatched mixed chimerism results in depleting host-type pre-existing pr

234 Induction of mixed hematopoietic chimerism results in donor-specific immunological tolera

235 compatibility complex (MHC)-mismatched mixed chimerism reversed autoimmunity and reestablished thymic

236 In patients with mixed chimerism, selective advantage for donor-derived T cells

237 consistently induced compartmentalized donor chimerism, (significant whole-blood chimerism, lacking T

238 ic T-cell numbers and select cells to assess chimerism status in a subset of R+/D- and R+/seropositiv

239 infections, and significantly influence the chimerism status toward recipients.

240 immunity and might therefore also influence chimerism status.

241 ost-HCT SCID patients, irrespective of their chimerism status.

242 However, these mixed-chimerism strategies were limited either by loss of long

243 A skin biopsy and chimerism study should be performed whenever possible.

244 At high levels of chimerism such protocols can permit central deletional t

245 as and generated chimeras with a higher skin chimerism than those derived from fiPSC.

246 ity of EVs and the existence of interspecies chimerism that characterizes the novel variants in the c

247 Upon cord blood full chimerism, the patient's CCR5 Delta32 homozygous CD4 T c

248 Hematopoietic chimerism, the stable coexistence of host and donor bloo

249 ayed tolerance induction strategy with mixed chimerism through BMT in prior kidney or VCA recipients.

250 zed composite allotransplantation (VCA) with chimerism through bone marrow transplantation (BMT) are

251 a/Fc, or IL-10/Fc fusion proteins to promote chimerism to induce tolerance.

252 signed to reveal the mechanisms on how mixed chimerism tolerizes autoreactive B cells in T1D.

253 NOD mice, but it is still unclear how mixed chimerism tolerizes autoreactive B cells.

254 h2/Th1 cytokine profile, conversion of mixed chimerism toward full donor chimerism, and a potentially

255 obin expression/VCN and enhanced early human chimerism under nonmyeloablative conditions, thus repres

256 Chimerism under yet lower irradiation (4.5Gy) was achiev

257 ed immune regulation in the context of mixed chimerism using a murine model of HLH.

258 Induction of mixed or complete chimerism via hematopoietic cell transplantation (HCT) f

259 Prolongation of transient porcine chimerism via transgenic expression of human CD47 in a p

260 em cell source, toxicity, engraftment, GVHD, chimerism, viral reactivation, post-HSCT complications,

261 Donor chimerism was achieved in 20% of recipients conditioned

262 Xenogeneic peripheral blood chimerism was assessed after each infusion.

263 Chimerism was associated with the generation of regulato

264 When split cell chimerism was available, 95% or more myeloid donor chime

265 - and B-cell immune reconstitution and donor chimerism was compared between the NK(+) (n = 24) and NK

266 The degree of donor LC-chimerism was correlated with the development of skin GV

267 Mixed chimerism was detected in peripheral blood at 1 month af

268 Stable (>/=90%) myeloid donor chimerism was documented in 52 (93%) surviving patients.

269 ism was available, 95% or more myeloid donor chimerism was documented in 80% of surviving patients.

270 torically performed sequentially after donor chimerism was established.

271 ogeneic HSCT, the rate of stable mixed-donor chimerism was high and allowed for complete replacement

272 Donor chimerism was indispensable for sustained tolerance, as

273 Accordingly, mixed chimerism was induced in NOD mice through radiation-free

274 Using this modified approach, mixed chimerism was induced successfully in 11 of 13 recipient

275 After delayed BMT, mixed chimerism was initially achieved in all KTx or VCA recip

276 n peripheral blood at 1 month after VCA, but chimerism was lost in all transplant recipients by 4 mon

277 Chimerism was lost in three patients at 2, 3, and 6 mont

278 Deletion did not persist when chimerism was lost.

279 This chimerism was not sufficient to prolong renal allograft

280 was delayed by two months, and full donor LC-chimerism was only reached by day 84 after transplant.

281 mixed chimerism, without significant T cell chimerism, was achieved in the animals that received BMT

282 B-lymphocyte and myeloid chimerism were highly correlated (rho, 0.98; P < .001).

283 type of conditioning, and presence of mixed chimerism were not.

284 gly, detectable levels of human CD45(+) cell chimerism were observed after transplantation of cord bl

285 either stable mixed chimerism or full donor chimerism were observed.

286 The level and duration of transient chimerism were substantially greater in baboons receivin

287 itted establishment of durable hematopoietic chimerism when the mice were given a low dose of donor B

288 ompared with naive T cells to increase donor chimerism when transferred to quiescent mixed allogeneic

289 d were comparable to subjects with transient chimerism who underwent autologous reconstitution.

290 th SCD allows for stable mixed hematopoietic chimerism with associated full-donor erythroid engraftme

291 refore, we tested whether induction of mixed chimerism with major histocompatibility complex (MHC)-ma

292 Induction of mixed chimerism with MHC-matched nonautoimmune donor BM transp

293 wever, induction of either mixed or complete chimerism with MHC-mismatched BM transplants prevented T

294 reactive T-cells, whereas induction of mixed chimerism with mismatched BM transplants did.

295 Strategies to achieve mixed chimerism with relatively low toxicity have significantl

296 2%, P < .01) and had high-level donor T-cell chimerism with superior long-term recovery of CD4 T-cell

297 Fifteen patients developed multilineage chimerism without graft-versus-host disease (GVHD), and

298 High-level mixed chimerism without GVHD can be achieved using MGMT transg

299 Tolerance induction by mixed chimerism without toxic conditioning and with a low risk

300 Transient mixed chimerism, without significant T cell chimerism, was ach