ライフサイエンスコーパス: graft-versus-host

1 ation, ie, very strong host-versus-graft and graft-versus-host alloresponses, which led respectively

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

18 55.1%, p < 0.001) and in those who developed graft-versus-host disease (47.9%, p < 0.001).

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

59 (15%), as were the rates of acute grade 2-4 graft-versus-host disease (GVHD) (21%).

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

79 1(-/-)donor T cells caused less severe acute graft-versus-host disease (GVHD) and yielded higher numb

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

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

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

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

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

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

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

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

88 7 accumulation resulting in severe pulmonary graft-versus-host disease (GVHD) following allogeneic he

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

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

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

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

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

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

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

96 1 blocking strategy can increase the risk of graft-versus-host disease (GVHD) in murine models.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

215 3, and grade 3-4 in 1, and moderate chronic graft-versus-host disease in 1 patient.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

295 host environment has critical effects on the graft-versus-host (GVH) responses mediated by naive dono

296 ainst retina cells represents a mechanism of graft-versus-host interaction following hematopoietic ce

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

298 The graft-versus-host reaction of CD4(+) T cells, but not of

299 tricted alloreactive T cell responses during graft-versus-host reaction, but failed to control autoim

300 anufactured with this process do not mediate graft-versus-host reactions and are rendered resistant t