ライフサイエンスコーパス: graft-versus-host disease

1 x 2(-/-) T cells were protected from severe graft versus host disease.

2 similar incidences of grades II to IV acute graft-versus host disease.

3 e on Criteria for Clinical Trials in Chronic Graft-Versus-Host Disease.

4 t can circumvent central tolerance and limit graft-versus-host disease.

5 ty and alloimmunity in models of colitis and graft-versus-host disease.

6 risks related to transplant conditioning and graft-versus-host disease.

7 n dermatitis, cutaneous T-cell lymphoma, and graft-versus-host disease.

8 n a mouse model of TCR gene transfer-induced graft-versus-host disease.

9 tuation of inflammatory processes, including graft-versus-host disease.

10 ll rejection of organ transplants and drives graft-versus-host disease.

11 ed immune cells can trigger life-threatening graft-versus-host disease.

12 alloresponses that cause graft rejection or graft-versus-host disease.

13 ferences were observed for acute and chronic graft-versus-host disease.

14 y and other factors such as neutropenia, and graft-versus-host disease.

15 iated with a higher risk of developing acute graft-versus-host disease.

16 cations such as infection and posttransplant graft-versus-host disease.

17 Ns in a preclinical model of sclerodermatous graft-versus-host disease.

18 rrow HCT and an increase in the incidence of graft-versus-host disease.

19 ved graft survival and decreased severity of graft-versus-host disease.

20 or safety reasons and concerns of triggering graft-versus-host disease.

21 o treat human lymphoid tumors and ameliorate graft-versus-host disease.

22 ee-survival, nonrelapse mortality (NRM), and graft-versus-host disease.

23 s of transplant protocols, or development of graft-versus-host disease.

24 vious cell therapy clinical trial to prevent graft-versus-host disease.

25 ventually remove the issues of rejection and graft-versus-host disease.

26 no acute toxicities or significant onset of graft-versus-host disease.

27 ity reprieving the allogeneic recipient from graft-versus-host disease.

28 utic agent for individuals with diabetes and graft-versus-host disease.

29 arsh conditioning, and do not have a risk of graft-versus-host disease.

30 ne inflammatory bowel disease and allogeneic graft-versus-host disease.

31 g regimens, corticosteroids, infections, and graft-versus-host disease.

32 ter accounting for immune reconstitution and graft-versus-host disease.

33 ic enterocolitis resembling acute intestinal graft-versus-host-disease.

34 ific antitumour immunity and pathogenesis of graft-versus-host diseases.

35 55.1%, p < 0.001) and in those who developed graft-versus-host disease (47.9%, p < 0.001).

36 Main causes of non-relapse mortality were graft-versus-host disease (49 [10%] in the intravenous b

37 ses including allograft rejection (6.69) and graft-versus-host disease (6.54).

38 ve at eradicating malignancy and often cause graft-versus-host disease, a potentially lethal immune r

39 iciently suppressed effector T cell-mediated graft-versus-host disease after allogeneic hematopoietic

40 New-onset acute graft-versus-host disease after CAR T-cell infusion deve

41 after solid-organ transplantation or prevent graft-versus-host disease after transfer of hematopoieti

42 expression in donor T cells may alter acute graft-versus-host disease (aGvHD) after allogeneic bone

43 Acute graft-versus-host disease (aGVHD) continues to be a freq

44 s have improved survival and decreased acute graft-versus-host disease (aGVHD) in 2 different murine

45 therapy for hematologic malignancies, acute graft-versus-host disease (aGVHD) is a leading cause of

46 We found that acute graft-versus-host disease (aGVHD) is associated with lym

47 Acute graft-versus-host disease (aGVHD) is the main complicati

48 Acute graft-versus-host disease (aGVHD) is the most common com

49 Acute intestinal graft-versus-host disease (aGVHD) refractory to immunosu

50 The incidence of acute graft-versus-host disease (aGVHD) was compared in patien

51 hematopoietic cell transplantation is acute graft-versus-host disease (aGVHD), a devastating conditi

52 in mice that had previously developed acute graft-versus-host-disease (aGVHD).

53 ious disease, cancer, regenerative medicine, graft-versus-host disease, allergies, and immunity.

54 Chronic graft-versus-host disease and an initial response to SCT

55 this mutein prolonged survival in a model of graft-versus-host disease and blocked spontaneous prolif

56 ), introduced to the conditioning to prevent graft-versus-host disease and graft failure, negatively

57 ll responses with important implications for graft-versus-host disease and graft-versus-leukemia.

58 for diagnosis and evaluation of treatment of graft-versus-host disease and holds promise for other di

59 of 44.5 months, two of 10 (20%) died due to graft-versus-host disease and infection, respectively.

60 clinical symptoms in animal models of acute graft-versus-host disease and multiple sclerosis.

61 Notch inhibition in T cells prevented graft-versus-host disease and organ rejection, establish

62 d more severe inflammatory bowel disease and graft-versus-host disease and produced higher levels of

63 man studies demonstrating Tregs can decrease graft-versus-host disease and vasculitides, there is con

64 against CMV infection as long as they had no graft-versus-host disease and/or were not receiving syst

65 kewing tumor growth data and the severity of graft versus host disease, and also increase the therape

66 at organ or bone-marrow allograft rejection, graft versus host disease, and autoimmune diseases.

67 ed T cell responses during organ transplant, graft-versus-host disease, and allergies are also major

68 Among patients receiving HCT, 27 (40%) had graft-versus-host disease, and most deaths occurred with

69 severe cortisone-resistant gastrointestinal graft-versus-host disease, and the patient died from mul

70 Strategies to prevent graft-versus-host disease are important as well because

71 ilable because immune complications, such as graft-versus-host disease, are greater without a matched

72 Active acute graft-versus-host disease at TMA diagnosis was the only

73 Chronic graft-versus-host disease (cGVHD) after allogeneic hemat

74 in (ATG) decreases the occurrence of chronic graft-versus-host disease (CGVHD) after haemopoietic cel

75 Novel therapies for chronic graft-versus-host disease (cGVHD) are needed.

76 eclinical and clinical research into chronic graft-versus-host disease (cGVHD) has come to fruition i

77 ssful treatment of older recipients, chronic graft-versus-host disease (cGVHD) has emerged as the maj

78 iation between HY-Ab development and chronic graft-versus-host disease (cGVHD) has yet to be elucidat

79 a lupus model, we induced lupus-like chronic graft-versus-host disease (cGVHD) in Stat1-knockout (KO)

80 tem cells, including a lower rate of chronic graft-versus-host disease (cGVHD) in the presence of inc

81 Chronic graft-versus-host disease (cGVHD) is a major cause of la

82 Chronic graft-versus-host disease (cGVHD) is a major complicatio

83 Chronic graft-versus-host disease (cGVHD) is a major complicatio

84 Chronic graft-versus-host disease (cGVHD) is a notorious complic

85 Chronic graft-versus-host disease (cGVHD) is a serious complicat

86 Chronic graft-versus-host disease (cGVHD) is an autoimmune-like

87 Chronic graft-versus-host disease (cGVHD) is associated with ina

88 nctions in the pathogenesis of cGVHD.Chronic graft-versus-host disease (cGVHD) is mediated by specifi

89 Chronic graft-versus-host disease (cGVHD) is the main cause of l

90 Although chronic graft-versus-host disease (CGVHD) is the primary nonrela

91 Chronic graft-versus-host disease (cGVHD) remains a major compli

92 Chronic graft-versus-host disease (cGVHD) remains a major late c

93 Chronic graft-versus-host disease (cGVHD) remains one of the mos

94 (Syk) inhibition for more effective chronic graft-versus-host disease (cGVHD) treatment.

95 hymocyte globulin-Fresenius) reduces chronic graft-versus-host disease (cGVHD) without compromising s

96 cells contribute to pathogenesis in chronic graft-versus-host disease (cGVHD), a condition manifeste

97 cell transplantation is hampered by chronic graft-versus-host disease (cGVHD), resulting in multiorg

98 tial pathological role of B cells in chronic graft-versus-host disease (cGVHD).

99 therapeutic effect in patients with chronic graft-versus-host disease (cGvHD).

100 Chronic graft-versus-host-disease (cGVHD) can cause multiorgan s

101 e effective in preventing the development of graft-versus-host disease compared with polyclonal Tregs

102 Patients <50 years old and without chronic graft-versus-host disease, compared with the remaining p

103 patients were assessed for the occurrence of graft-versus-host disease, death, and major functional d

104 r caused by acid reflux, allergic responses, graft-versus-host disease, drugs, or infections, is a co

105 ytopenias) was reported in 4 patients, acute graft-versus-host disease grade 1 in 2, grade 2 in 3, an

106 re safe, and only two occurrences of de novo graft-versus host disease (grade 1) were observed.

107 Chronic graft versus host disease (GVHD) is a major cause of mor

108 Graft versus Host Disease (GvHD) remains one of the main

109 re and after transplant, eliminates risks of graft versus host disease (GVHD), and, as the authors re

110 ey influence disease processes such as acute graft versus host disease (GVHD), which is the main comp

111 second-line treatment for acute and chronic graft versus host disease (GVHD).

112 A history of graft-versus-host disease (GVHD) ( n = 27) was associate

113 (15%), as were the rates of acute grade 2-4 graft-versus-host disease (GVHD) (21%).

114 sed the cumulative incidence (CI) of chronic graft-versus-host disease (GvHD) (hazards ratio [HR], 0.

115 ence, nonrelapse mortality, and incidence of graft-versus-host disease (GVHD) after allo-HSCT.

116 ressive therapy required to prevent or treat graft-versus-host disease (GVHD) after allogeneic blood

117 ory T cells (Tregs) can control experimental graft-versus-host disease (GVHD) after allogeneic hemato

118 s (SNPs) associated with the risk of chronic graft-versus-host disease (GVHD) after allogeneic hemato

119 +) regulatory T cells (T reg cells) suppress graft-versus-host disease (GvHD) after allogeneic hemato

120 mbotic microangiopathy to steroid-refractory graft-versus-host disease (GVHD) after allogeneic stem-c

121 ve, with 8 (26%) deaths related to new-onset graft-versus-host disease (GVHD) after anti-PD-1.

122 to enhance immune reconstitution and prevent graft-versus-host disease (GVHD) after hematopoietic ste

123 s safe and results in low incidence of acute graft-versus-host disease (GVHD) after reduced-intensity

124 t and IFN-gamma in T cell responses in acute graft-versus-host disease (GVHD) and found that T-bet(-/

125 a major cause of morbidity and mortality in graft-versus-host disease (GVHD) and is attributable to

126 with significant complications, principally graft-versus-host disease (GVHD) and opportunistic infec

127 Graft-versus-host disease (GVHD) and posttransplant immu

128 strategies are used to mitigate the risk of graft-versus-host disease (GvHD) and rejection associate

129 However, graft-versus-host disease (GVHD) and relapse after allo-

130 had a reduced incidence and delayed onset of graft-versus-host disease (GVHD) and significantly prolo

131 ial role of TNF and intestinal cell death in graft-versus-host disease (GVHD) and the ability of TWEA

132 biota health and predicts reduced intestinal graft-versus-host disease (GVHD) and treatment-related m

133 1(-/-)donor T cells caused less severe acute graft-versus-host disease (GVHD) and yielded higher numb

134 rted that donor effector T-cell function and graft-versus-host disease (GVHD) are regulated via recip

135 rine model of acute and chronic (lupus-like) graft-versus-host disease (GVHD) as models of a CTL-medi

136 ission after RIC, we hypothesize that higher graft-versus-host disease (GVHD) associated with PB tran

137 The incidence of grade II-IV acute graft-versus-host disease (GVHD) at 100 days was 9% (95%

138 wn to be critical for CD8(+) T cell-mediated graft-versus-host disease (GVHD) but dispensable for GVH

139 ransiently secrete interleukin (IL)-17 cause graft-versus-host disease (GVHD) but do not contribute t

140 d outcomes in patients with gastrointestinal graft-versus-host disease (GVHD) by measuring 23 biomark

141 y T cells (TEM) are less capable of inducing graft-versus-host disease (GVHD) compared with naive T c

142 d immune reconstitution and if any resultant graft-versus-host disease (GVHD) could be controlled by

143 7 accumulation resulting in severe pulmonary graft-versus-host disease (GVHD) following allogeneic he

144 al targets for the therapy and prevention of graft-versus-host disease (GVHD) following allogeneic he

145 of 9 transplant recipients experienced acute graft-versus-host disease (GVHD) following aNK-DLI, with

146 Cumulative incidence (day +90) of acute graft-versus-host disease (GVHD) grade 2-4 was 21%.

147 Acute graft-versus-host disease (GVHD) grades 2-4 was more fre

148 Treatment of acute graft-versus-host disease (GVHD) has evolved from a one-

149 lls also mediated accelerated onset of acute graft-versus-host disease (GVHD) in a murine model, char

150 Azacitidine (AzaC) mitigates graft-versus-host disease (GvHD) in both murine preclini

151 1 blocking strategy can increase the risk of graft-versus-host disease (GVHD) in murine models.

152 ities have been associated with an increased graft-versus-host disease (GVHD) incidence, and the MICA

153 The development of graft-versus-host disease (GVHD) is a common complicatio

154 Graft-versus-host disease (GVHD) is a complication of al

155 Graft-versus-host disease (GVHD) is a complication of al

156 Sclerotic graft-versus-host disease (GVHD) is a distinctive phenot

157 Acute graft-versus-host disease (GvHD) is a life-threatening c

158 Graft-versus-host disease (GvHD) is a life-threatening i

159 Graft-versus-host disease (GVHD) is a major cause of mor

160 Graft-versus-host disease (GVHD) is a major cause of mor

161 Graft-versus-host disease (GVHD) is a major cause of mor

162 Acute graft-versus-host disease (GvHD) is a major complication

163 in hematologic malignancies, but the risk of graft-versus-host disease (GVHD) is a major limitation f

164 Graft-versus-host disease (GVHD) is a severe complicatio

165 Graft-versus-host disease (GVHD) is common after allogen

166 The risk of acute graft-versus-host disease (GVHD) is higher after allogen

167 However, graft-versus-host disease (GVHD) is mediated by the same

168 metabolites and on disease processes such as graft-versus-host disease (GVHD) is not known.

169 (ICU) remains controversial, especially when graft-versus-host disease (GVHD) is present.

170 Chronic graft-versus-host disease (GVHD) is the leading cause of

171 Graft-versus-host disease (GVHD) is the major cause of n

172 Graft-versus-host disease (GVHD) is the major limitation

173 Lower gastrointestinal (GI) tract graft-versus-host disease (GVHD) is the predominant caus

174 However, graft-versus-host disease (GVHD) may develop when donor-

175 oth radiation exposure during transplant and graft-versus-host disease (GVHD) may increase risk of la

176 efficacy of HuMoSCs was evaluated by using a graft-versus-host disease (GvHD) model of humanized mice

177 d the participation of the 5-LO/LTB4 axis in graft-versus-host disease (GVHD) pathogenesis by transpl

178 provide encouragement that important chronic graft-versus-host disease (GVHD) patient outcomes (such

179 Sir) vs tacrolimus/methotrexate (Tac/Mtx) as graft-versus-host disease (GVHD) prophylaxis after match

180 f posttransplant cyclophosphamide (PT-Cy) as graft-versus-host disease (GVHD) prophylaxis has revolut

181 Graft-versus-host disease (GVHD) prophylaxis included ca

182 The haploidentical group received graft-versus-host disease (GVHD) prophylaxis with PT-Cy

183 ceived posttransplant cyclophosphamide-based graft-versus-host disease (GVHD) prophylaxis, whereas UR

184 en and posttransplant cyclophosphamide-based graft-versus-host disease (GVHD) prophylaxis.

185 stem cell transplantation (HSCT) and enteric graft-versus-host disease (GVHD) remain unexplored.

186 Chronic graft-versus-host disease (GVHD) remains a common and po

187 splantation continue to improve, but chronic graft-versus-host disease (GVHD) remains a common toxici

188 Despite major advances in recent years, graft-versus-host disease (GVHD) remains a major life-th

189 Intestinal graft-versus-host disease (GVHD) remains a significant o

190 Treatment of steroid-resistant acute graft-versus-host disease (GVHD) remains an unmet clinic

191 en is presented to donor T cells to generate graft-versus-host disease (GVHD) represents an attractiv

192 Graft-versus-host disease (GVHD) represents the major no

193 l Institutes of Health (NIH)-defined chronic graft-versus-host disease (GVHD) requiring systemic trea

194 We show that B7-H3 is upregulated in graft-versus-host disease (GVHD) target organs, includin

195 gnature of T cells during breakthrough acute graft-versus-host disease (GVHD) that occurs in the sett

196 eath, were observed in 6 patients (21%), and graft-versus-host disease (GVHD) that precluded further

197 s from third-party mice protects from lethal graft-versus-host disease (GVHD) through expansion of do

198 er vitamin A levels would reduce the risk of graft-versus-host disease (GVHD) through reduced gastroi

199 Overall incidences of graft-versus-host disease (GVHD) were similar, but chron

200 regs) have been shown to effectively prevent graft-versus-host disease (GVHD) when adoptively transfe

201 s recognize host tissues as foreign, causing graft-versus-host disease (GVHD) which is a main contrib

202 tem cell transplantation (HSCT), controlling graft-versus-host disease (GVHD) while maintaining graft

203 rived regulatory T cells (Tregs) may prevent graft-versus-host disease (GVHD) while preserving graft-

204 Alloimmune T cell responses induce graft-versus-host disease (GVHD), a serious complication

205 nt in trials of initial treatment of chronic graft-versus-host disease (GVHD), and evidence showing t

206 cell transplantation (allo-HCT) are relapse, graft-versus-host disease (GVHD), and infection.

207 agnosis includes drug reactions, infections, graft-versus-host disease (GVHD), and mixed diseases.

208 rged as a strategy to reduce the severity of graft-versus-host disease (GVHD), and recalibrate the ef

209 ses, which led respectively to rejection and graft-versus-host disease (GVHD), being overcome through

210 ally corrected cells would avoid the risk of graft-versus-host disease (GVHD), but the genotoxicity o

211 Blockade of PD-1 increases the severity of graft-versus-host disease (GVHD), but the interplay betw

212 dvanced understanding of histocompatibility, graft-versus-host disease (GVHD), GVL effect, and immune

213 (IL-17A) can mediate late immunopathology in graft-versus-host disease (GVHD), however protective rol

214 Complications include graft failure, graft-versus-host disease (GVHD), infection, and transpl

215 essed as individual complications, including graft-versus-host disease (GVHD), relapse, or death, yet

216 the pathogenesis of intestinal mucositis and graft-versus-host disease (GVHD), these cytokines are co

217 rum of patients developing acute and chronic graft-versus-host disease (GVHD), we reasoned that inhib

218 has been shown to exacerbate the severity of graft-versus-host disease (GVHD), whereas costimulation

219 ls are the driving force in the induction of graft-versus-host disease (GVHD), yet little is known ab

220 tion (SCT), using the composite end point of graft-versus-host disease (GVHD)-free and progression-fr

221 tact hypersensitivity (CHS) and experimental graft-versus-host disease (GVHD)-like disease.

222 ved between groups in the incidence of acute graft-versus-host disease (GVHD).

223 host normal tissues through the often fatal graft-versus-host disease (GVHD).

224 dels of inflammatory bowel disease and acute graft-versus-host disease (GVHD).

225 damage healthy tissues resulting in harmful graft-versus-host disease (GVHD).

226 mising treatment for allograft rejection and graft-versus-host disease (GVHD).

227 host target tissues reduces the incidence of graft-versus-host disease (GVHD).

228 h leukemia but have the potential to mediate graft-versus-host disease (GVHD).

229 d with the subsequent development of chronic graft-versus-host disease (GVHD).

230 severity in inflammatory diseases, including graft-versus-host disease (GVHD).

231 of a PD-1H agonistic mAb protected mice from graft-versus-host disease (GVHD).

232 ansplantation (allo-HCT) is limited by acute graft-versus-host disease (GVHD).

233 loss of long-term mixed chimerism or risk of graft-versus-host disease (GVHD).

234 ders but carries a significant risk of acute graft-versus-host disease (GVHD).

235 e and potentially lethal inflammation called graft-versus-host disease (GVHD).

236 eatening infections and an increased risk of graft-versus-host disease (GVHD).

237 fferentiate between relapse and the onset of graft-versus-host disease (GVHD).

238 tial cause of impaired antiviral immunity in graft-versus-host disease (GVHD).

239 o augment graft-versus-tumor effects without graft-versus-host disease (GVHD).

240 th in vitro and in multiple murine models of graft-versus-host disease (GVHD).

241 ith increased mortality and gastrointestinal graft-versus-host disease (GVHD).

242 stem cell transplantation resulting in acute graft-versus-host disease (GVHD).

243 kemia (GVL) reactivity, with a lower risk of graft-versus-host disease (GVHD).

244 les are associated with an increased risk of graft-versus-host disease (GVHD).

245 was used for preventing graft rejection and graft-versus-host disease (GVHD); no patient received an

246 Graft-versus-host-disease (GVHD) after liver transplanta

247 None of the 27 patients developed graft-versus-host-disease (GVHD) following ibrutinib ini

248 matopoietic stem cell transplantation, acute graft-versus-host-disease (GVHD) is caused by an attack

249 Mixed chimerism and graft-versus-host-disease (GVHD) remain limitations on s

250 te toxicity (veno-occlusive disease or acute graft versus-host disease [GvHD]); chronic GvHD; overall

251 The patients who developed acute or chronic graft-versus-host disease had a longer overall survival

252 No treatment-related death or graft-versus-host disease had been reported; 15 of the 1

253 upportive care, and prevention/management of graft-versus-host disease have expanded stem cell transp

254 associated with decreased incidence of acute graft-versus-host disease (hazard ratio [HR], 0.31; 95%

255 The CI of acute graft-versus-host disease II to IV was 32.3% after RIC a

256 n trials have shown benefits in treatment of graft versus host disease in matched or mismatched stem

257 3, and grade 3-4 in 1, and moderate chronic graft-versus-host disease in 1 patient.

258 ere present in 50% of the patients and acute graft-versus-host disease in 33%.

259 reg cells in association with clinical acute graft-versus-host disease in allogeneic hematopoietic ce

260 cells are central mediators of rejection and graft-versus-host disease in both solid organ and hemato

261 munization with OVA and induction of chronic graft-versus-host disease in female ERalpha-knockout mic

262 Four patients had graft-versus-host disease in the 45 days after VST infus

263 ity was observed, except for a grade II skin graft-versus-host disease in the patient treated for hem

264 interval, 1.84-31.7), controlling for acute graft-versus-host disease, in 109 patients with Philadel

265 t-related mortality (TRM), acute and chronic graft-versus-host disease incidence and severity, time t

266 ut toxic conditioning and with a low risk of graft versus host disease is a visionary but realistic g

267 s-host disease prophylaxis and in refractory graft-versus-host disease is associated with improved su

268 t in vivo alloresponses using a severe acute graft versus host disease model.

269 of IFNgamma-secreting Tregs in a xenogeneic graft-versus-host disease model and in adoptive transfer

270 ratio, 2.14; 95% CI, 1.88-2.45) and without graft-versus-host disease (odds ratio, 1.35; 95% CI, 1.1

271 poietic stem cell transplant recipients with graft-versus-host disease (odds ratio, 2.14; 95% CI, 1.8

272 topoietic stem cell transplantation, chronic graft versus host disease of the lung manifests most fre

273 ; P = .04) without a significant increase in graft-versus-host disease or nonrelapse mortality.

274 (P = 0.004, hazard ratio = 8.2) and chronic graft-versus-host disease (P = 0.010, hazard ratio = 5.3

275 secondary Sjogren's disease (P = 0.08), and graft-versus-host disease (P = 0.04).

276 d HCT, myeloablative conditioning, and acute graft-versus-host disease (P values < .01).

277 Our findings were confirmed in T-cells from graft-versus-host disease patients treated with extracor

278 the sequence of therapeutic classes used in graft-versus-host disease prophylaxis and in refractory

279 s given at a cumulative dose of 8 mg/kg, and graft-versus-host disease prophylaxis was composed of cy

280 th cyclophosphamide (CY; days -2 and +2) for graft-versus-host disease prophylaxis, and 1.5 x 10(7) h

281 Grade II to IV acute graft-versus-host disease related to steroid treatment s

282 Acute and chronic graft-versus-host disease remain important complications

283 However, organ rejection and graft-versus-host disease remain major obstacles to the

284 the overexpression of IFN-inducible genes in graft-versus-host disease skin and markedly reduced derm

285 get tissue damage in a unique in vitro human graft-versus-host disease skin explant model.

286 Therapy for steroid-refractory acute graft-versus-host disease (SR-aGVHD) remains suboptimal.

287 Transfusion-associated graft-versus-host disease (TA-GVHD) is a rare complicati

288 tumor rejection without inducing xenogeneic graft-versus-host disease, thus resulting in significant

289 in trials to control allograft rejection and graft versus host disease.Thymic-derived Treg cells with

290 vation including age >/=50 years and chronic graft-versus-host disease; treatment strategies based on

291 he incidence of grades 2-4 acute and chronic graft-versus-host disease was 20% and 10%, respectively.

292 umulative incidence of grade III to IV acute graft-versus-host disease was 36% by D+100.

293 The CI of chronic graft-versus-host disease was 61.6% after RIC and 64.7%

294 No unexpected toxicity or graft-versus-host disease was observed.

295 ies of nonrelapse mortality and severe acute graft-versus-host disease were 8% and 4%.

296 ; P < .001) and chronic (HR, 0.35; P < .001) graft-versus-host disease were lower with transplantatio

297 te or late toxicities and no exacerbation of graft-versus-host disease were observed.

298 However, 3 dogs developed graft-versus-host disease, whereas 1 dog rejected its st

299 ations were predictors for the occurrence of graft-versus-host disease, whereas CMV and BK virus reac

300 IT-901 suppressed graft-versus-host disease while preserving graft-versus-