ライフサイエンスコーパス: graft-versus-host

1 for steroid-dependent or -refractory chronic graft-versus-host diesease (cGVHD) are poor, and only ib

2 d loss of diversity correlates with acute GI graft versus host disease (GvHD) and poor outcomes.

3 models, including organ transplantation and graft versus host disease (GVHD) but they have limitatio

4 ls testing prevention strategies for chronic graft versus host disease (GVHD) have measured its cumul

5 Severe pulmonary chronic graft versus host disease (GVHD) is a life-threatening c

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

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

8 In intestinal transplantation, graft versus host disease (GVHD), while relatively rare,

9 cipients expired by day 40 from severe acute graft versus host disease (GVHD).

10 morbidity and mortality rates, mainly due to graft versus host disease (GvHD).

11 lyl glycine (DMOG) in the pathophysiology of graft versus host disease (GVHD).

12 lymphoproliferative disorder (P = 0.09) and graft versus host disease (P = 0.002).

13 seases(1), including steroid-resistant acute graft versus host disease (SR-aGvHD)(2).

14 vention and treatments for acute and chronic graft versus host disease after transplantation.

15 tors for its occurrence were the presence of graft versus host disease and the use of alemtuzumab.

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

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

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

19 reinduction or consolidation chemotherapy or graft versus host disease treatment in hematopoietic ste

20 hymocyte antiglobulin, and acute and chronic graft versus host disease were significantly associated

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

22 l for use as models for allotransplantation, graft versus host disease, and regenerative medicine.

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

24 graftment is development of acute xenogeneic graft- versus-host disease (GVHD) due to human T-cell re

25 Lack of acute xenogeneic graft- versus-host disease, but retention of T-cell func

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

27 atients who develop steroid-refractory acute graft-versus-host disease (aGVHD) after allogeneic hemat

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

29 were followed for disease relapse and acute graft-versus-host disease (aGvHD) development post-HSCT.

30 Acute graft-versus-host disease (aGVHD) hinders the efficacy o

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

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

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

34 nt of severe and/or steroid-refractory acute graft-versus-host disease (aGVHD) remains a significant

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

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

37 ion viral reactivation, grade II to IV acute graft-versus-host disease (aGvHD), and chronic graft-ver

38 ressor cells (MDSCs) in the setting of acute graft-versus-host disease (aGVHD).

39 is connected to a higher incidence of acute graft-versus-host disease (aGVHD).

40 1.50-5.55; P = 0.002) and grade II-IV acute graft-versus-host disease (aHR, 1.59; 95% CI, 1.06-2.39;

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

42 Chronic graft-versus-host disease (cGVHD) and late acute graft-v

43 injury attributable to experimental chronic graft-versus-host disease (cGVHD) by targeting B-cell ly

44 aft-versus-host disease (aGvHD), and chronic graft-versus-host disease (cGvHD) complicated 49.6%, 35%

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

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

47 Chronic graft-versus-host disease (cGVHD) is a leading cause of

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

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

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

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

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

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

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

55 Chronic graft-versus-host disease (cGVHD) represents a double-ed

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

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

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

59 y complications in a murine model of chronic graft-versus-host disease (cGVHD).

60 ic autoimmune-like syndrome known as chronic graft-versus-host disease (cGVHD).

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

62 Chronic pulmonary graft-versus-host disease (cpGVHD) after hematopoietic c

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

64 (15%), as were the rates of acute grade 2-4 graft-versus-host disease (GVHD) (21%).

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

66 Graft-versus-host disease (GVHD) after allogeneic stem c

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

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

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

70 th life-threatening complications, including graft-versus-host disease (GVHD) and infections, which a

71 ococcal expansion, which was associated with graft-versus-host disease (GVHD) and mortality.

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

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

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

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

76 Secondary outcomes included graft-versus-host disease (GVHD) and relapse.

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

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

79 e cumulative incidence of grade 2 to 4 acute graft-versus-host disease (GVHD) at day 100 was 44%, and

80 Human graft-versus-host disease (GVHD) biology beyond 3 months

81 ions contributed to significant reduction in graft-versus-host disease (GVHD) but retained sufficient

82 e colony-stimulating factor (GM-CSF) promote graft-versus-host disease (GVHD) by recruiting donor den

83 Acute graft-versus-host disease (GVHD) can affect the central

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

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

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

87 A higher incidence of graft-versus-host disease (GVHD) has been observed after

88 occurred in 26 patients (16%), severe acute graft-versus-host disease (GVHD) in 9 (6%), and chronic

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

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

91 1 blocking strategy can increase the risk of graft-versus-host disease (GVHD) in murine models.

92 Graft-versus-host disease (GVHD) in the gastrointestinal

93 We have shown that under acute graft-versus-host disease (GVHD) inflammatory conditions

94 Graft-versus-host disease (GvHD) is a common complicatio

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

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

97 Acute graft-versus-host disease (GVHD) is a frequent complicat

98 Intestinal graft-versus-host disease (GVHD) is a life-threatening c

99 Acute graft-versus-host disease (GVHD) is a life-threatening c

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

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

102 Chronic graft-versus-host disease (GVHD) is a major complication

103 Graft-versus-host disease (GvHD) is a major complication

104 Graft-versus-host disease (GVHD) is a major factor contr

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

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

107 Acute graft-versus-host disease (GVHD) is initially triggered

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

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

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

111 Graft-versus-host disease (GVHD) is the most serious com

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

113 Yet, our understanding of how PTCy prevents graft-versus-host disease (GVHD) largely has been extrap

114 dence pointing to exacerbation of underlying graft-versus-host disease (GVHD) linked to presence of h

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

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

117 Gastrointestinal acute graft-versus-host disease (GVHD) occurring after allogen

118 whether the patient has or has not developed graft-versus-host disease (GvHD) or received immunosuppr

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

120 -based tools may identify a lower-risk acute graft-versus-host disease (GVHD) population amenable to

121 Graft-versus-host disease (GvHD) presents a major cause

122 Despite graft-versus-host disease (GVHD) prophylactic agents, th

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

124 ne (CSP) and mycophenolate mofetil (MMF) for graft-versus-host disease (GVHD) prophylaxis after nonmy

125 While tacrolimus and sirolimus (T/S)-based graft-versus-host disease (GvHD) prophylaxis has been ef

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

127 ATG) has represented the standard of care in graft-versus-host disease (GVHD) prophylaxis in patients

128 transplantation from haploidentical donors; graft-versus-host disease (GVHD) prophylaxis included po

129 We used post-transplant cyclophosphamide as graft-versus-host disease (GVHD) prophylaxis to expand d

130 cells as the source of the graft and PTCy as graft-versus-host disease (GvHD) prophylaxis.

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

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

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

134 Acute graft-versus-host disease (GVHD) remains a major limitat

135 Graft-versus-host disease (GVHD) remains a major limitat

136 Acute graft-versus-host disease (GVHD) remains a major obstacl

137 Graft-versus-host disease (GVHD) remains an important ca

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

139 Graft-versus-host disease (GVHD) remains one of the majo

140 s been driven by the premise that persistent graft-versus-host disease (GVHD) results from inadequate

141 tic accuracy of cGVHD and to better classify graft-versus-host disease (GVHD) syndromes but have not

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

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

144 Prevention of graft-versus-host disease (GvHD) without malignant relap

145 Graft-versus-host disease (GVHD), a common complication

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

147 relapse mortality, and severe (grade 3 or 4) graft-versus-host disease (GVHD), all evaluated through

148 including inflammatory bowel disease (IBD), graft-versus-host disease (GVHD), and cancer.

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

150 progression-free survival, acute and chronic graft-versus-host disease (GVHD), and GVHD-free and rela

151 immunologic mismatch can also lead to lethal graft-versus-host disease (GVHD), and immunosuppression

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

153 or cause of morbidity and mortality in acute graft-versus-host disease (GVHD), and pathological damag

154 s associated with a high risk of graft loss, graft-versus-host disease (GvHD), and transplant-related

155 tation is associated with excessive rates of graft-versus-host disease (GVHD), but AZA has been shown

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

157 Graft-versus-host disease (GVHD), however, remains one o

158 entrations are elevated in steroid-resistant graft-versus-host disease (GVHD), implying endothelial h

159 cases at the highest dose in the absence of graft-versus-host disease (GVHD), neurotoxicity, or dose

160 e was no impact of EBV reactivation on acute graft-versus-host disease (GVHD), nonrelapse mortality,

161 y as observed in a mouse model of intestinal graft-versus-host disease (GVHD), providing a roadmap fo

162 allogeneic immune-mediated gastrointestinal graft-versus-host disease (GVHD), the principal toxicity

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

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

165 tic cell transplantation (HCT) is limited by graft-versus-host disease (GVHD), which is the main post

166 nal microbiome-dependent metabolite, worsens graft-versus-host disease (GVHD).

167 gressive immunosuppression to better control graft-versus-host disease (GvHD).

168 he toxicity of preconditioning therapies and graft-versus-host disease (GVHD).

169 vaccine or a fourth PCV dose in the case of graft-versus-host disease (GvHD).

170 sory nerve damage in a mouse model of ocular graft-versus-host disease (GVHD).

171 amide expanded the donor pool while limiting graft-versus-host disease (GVHD).

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

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

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

175 ed allo-immune responses will lead to lethal graft-versus-host disease (GVHD).

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

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

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

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

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

181 contributes to pathology in animal models of graft-versus-host disease (GVHD).

182 it Itpkb signaling as a means of controlling graft-versus-host disease (GVHD).

183 papular rash on the skin was consistent with graft-versus-host disease (GVHD).

184 (PSV23) or a fourth PCV dose in the case of graft-versus-host disease (GvHD).

185 lications, predominantly infection and acute graft-versus-host disease (GVHD).

186 ological malignancies but remains limited by graft-versus-host disease (GVHD).

187 +/CD19+ graft depletion effectively prevents graft-versus-host disease (GVHD).

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

189 t-versus-host disease (cGVHD) and late acute graft-versus-host disease (L-aGVHD) are understudied com

190 lymphocytic leukemia (P = 0.02), and chronic graft-versus-host disease (P = 0.0002).

191 -versus-host disease (P = 0.03), and chronic graft-versus-host disease (P = 0.003).

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

193 ced-intensity conditioning (P = 0.02), acute graft-versus-host disease (P = 0.03), and chronic graft-

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

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

196 teroid-resistant or steroid-refractory acute graft-versus-host disease (SR-aGVHD) poses one of the mo

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

198 lycosyltransferase gene in T cells mediating graft-versus-host disease after allogeneic bone marrow t

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

200 These populations correlate with acute graft-versus-host disease after allogeneic hematopoietic

201 trials to alleviate autoimmune diseases and graft-versus-host disease after hematopoietic stem cell

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

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

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

205 eneic CAR T cells may cause life-threatening graft-versus-host disease and may be rapidly eliminated

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

207 amide is associated with low rates of severe graft-versus-host disease and nonrelapse mortality and d

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

209 ecreased after transplant in the presence of graft-versus-host disease and were not replaced, owing t

210 splantation without steroid-refractory acute graft-versus-host disease and without early relapse.

211 This study also supports chronic graft-versus-host disease as a risk factor for nonmelano

212 Post-transplant severe graft-versus-host disease could be improved, and earlier

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

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

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

216 3, and grade 3-4 in 1, and moderate chronic graft-versus-host disease in 1 patient.

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

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

219 enhancing T cell regeneration and mitigating graft-versus-host disease in HSCT.

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

221 in eight patients (38%), grade 1 acute skin graft-versus-host disease in two patients (10%), and gra

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

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

224 ic stem cell transplantation, with grade 3-4 graft-versus-host disease observed in five (26%).

225 rrow-liver-thymus (BLT) mouse model prone to graft-versus-host disease occurred only following revers

226 CT recipients without increasing the risk of graft-versus-host disease or disease relapse.

227 tion, cyclophosphamide, and fludarabine) and graft-versus-host disease prophylaxis (calcineurin inhib

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

229 h adult unrelated donors, using conventional graft-versus-host disease prophylaxis.

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

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

232 donor CD8(+) T cells (T(TCR-C4)) to minimize graft-versus-host disease risk and enhance transferred T

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

234 ose receiving systemic immunosuppression for graft-versus-host disease treatment.

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

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

237 In multivariate analysis, chronic graft-versus-host disease was a significant risk factor

238 Worsening graft-versus-host disease was not identified among Allo

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

240 cyte count <300 cells/uL at D +30, and acute graft-versus-host disease were predictors of ADV viremia

241 is associated with morbidity, rejection and graft-versus-host disease(2).

242 accompanied by morbidity and mortality from graft-versus-host disease(5).

243 including hepatitis B virus infection(5-7), graft-versus-host disease(8) and inflammatory bowel dise

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

245 posttransplant lymphoproliferative disorder, graft-versus-host disease, and enteric infections.

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

247 , invasive mold infection, acute and chronic graft-versus-host disease, and prednisone exposure.

248 cytokine release syndrome, neurotoxicity, or graft-versus-host disease, and there was no increase in

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

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

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

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

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

254 s inflammatory episodes, or acute or chronic graft-versus-host disease, occurred in any patient.

255 nt among patients who developed severe acute graft-versus-host disease, suggesting that short telomer

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

257 d can lead to inflammatory disorders such as graft-versus-host disease, transplant rejection and auto

258 t conditions such as hepatitis C vasculitis, graft-versus-host disease, type 1 diabetes, and systemic

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

260 oth patients were alive, without evidence of graft-versus-host disease, with major infection at 1 yea

261 ASIX) was shown to predict death after acute graft-versus-host disease.

262 He experienced mild gut graft-versus-host disease.

263 emic bacterial infection, colitis, and acute graft-versus-host disease.

264 syndrome-like phenotype and aggravated acute graft-versus-host disease.

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

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

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

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

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

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

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

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

273 eneic CAR T cells with limited potential for graft-versus-host disease.

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

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

276 None had grade III-IV acute or chronic graft-versus-host disease.

277 One patient developed grade I skin graft-versus-host disease.

278 with reduced survival and increased chronic graft-versus-host disease.

279 utoimmune diseases, transplant rejection and graft-versus-host disease.

280 rm of CD43 in multiple T cell subsets during graft-versus-host disease.

281 of the effector cells, but carry the risk of graft-versus-host disease.

282 and tissue manifestations of T-cell-mediated graft-versus-host disease.

283 marrow might promote graft immunogenicity or graft-versus-host disease.

284 stay; intensive care unit admissions; acute graft-versus-host disease; Bearman toxicity score; sinus

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

286 age at transplantation; steroid use, chronic graft-versus-host disease; use of fludarabine, melphalan

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

288 Acute graft-versus-host-disease (GVHD) after non-myeloablative

289 1 therapy reported substantial toxicity from graft-versus-host-disease (GVHD).

290 excellent graft function after overcoming a graft-versus-host-disease episode 5 months posttransplan

291 ace/ethnicity, malignant disease, graft, and graft-versus-host-disease prophylaxis), ST2 remained ass

292 myelofibrosis and show promising results in graft-versus-host-disease.

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

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

295 nucleotide polymorphisms (SNPs) that produce graft-versus-host (GVH) amino acid coding differences be

296 Graft-versus-host (GvH) disease (GvHD) remains a serious

297 al tolerance, but with a significant risk of graft-versus-host (GVH) disease (GVHD).

298 weight loss, human malignancies, or systemic graft-versus-host (GVH) disease were observed.

299 s in BLT mice that spontaneously developed a graft-versus-host-like condition, characterized by alope

300 as critical sources of Delta-like ligands in graft-versus-host responses irrespective of conditioning