ライフサイエンスコーパス: versus host

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

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

3 Chronic graft versus host disease (GVHD) is a major cause of morbidity

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

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

6 luence disease processes such as acute graft versus host disease (GVHD), which is the main complicati

7 d-line treatment for acute and chronic graft versus host disease (GVHD).

8 ls have shown benefits in treatment of graft versus host disease in matched or mismatched stem cell t

9 ic conditioning and with a low risk of graft versus host disease is a visionary but realistic goal.

10 ivo alloresponses using a severe acute graft versus host disease model.

11 tic stem cell transplantation, chronic graft versus host disease of the lung manifests most frequentl

12 tumor growth data and the severity of graft versus host disease, and also increase the therapeutic r

13 an or bone-marrow allograft rejection, graft versus host disease, and autoimmune diseases.

14 ar incidences of grades II to IV acute graft-versus host disease.

15 /-) T cells were protected from severe graft versus host disease.

16 als to control allograft rejection and graft versus host disease.Thymic-derived Treg cells with speci

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

18 n causes of non-relapse mortality were graft-versus-host disease (49 [10%] in the intravenous busulfa

19 cluding allograft rejection (6.69) and graft-versus-host disease (6.54).

20 ssion in donor T cells may alter acute graft-versus-host disease (aGvHD) after allogeneic bone marrow

21 Acute graft-versus-host disease (aGVHD) continues to be a frequent a

22 improved survival and decreased acute graft-versus-host disease (aGVHD) in 2 different murine alloge

23 py for hematologic malignancies, acute graft-versus-host disease (aGVHD) is a leading cause of transp

24 We found that acute graft-versus-host disease (aGVHD) is associated with lymphangi

25 Acute graft-versus-host disease (aGVHD) is the main complication of

26 Acute graft-versus-host disease (aGVHD) is the most common complicat

27 Acute intestinal graft-versus-host disease (aGVHD) refractory to immunosuppress

28 The incidence of acute graft-versus-host disease (aGVHD) was compared in patients wit

29 opoietic cell transplantation is acute graft-versus-host disease (aGVHD), a devastating condition tha

30 Chronic graft-versus-host disease (cGVHD) after allogeneic hematopoiet

31 G) decreases the occurrence of chronic graft-versus-host disease (CGVHD) after haemopoietic cell tran

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

33 cal and clinical research into chronic graft-versus-host disease (cGVHD) has come to fruition in the

34 treatment of older recipients, chronic graft-versus-host disease (cGVHD) has emerged as the major cau

35 between HY-Ab development and chronic graft-versus-host disease (cGVHD) has yet to be elucidated.

36 s model, we induced lupus-like chronic graft-versus-host disease (cGVHD) in Stat1-knockout (KO) and w

37 lls, including a lower rate of chronic graft-versus-host disease (cGVHD) in the presence of increased

38 Chronic graft-versus-host disease (cGVHD) is a major cause of late mor

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

40 Chronic graft-versus-host disease (cGVHD) is a major complication of h

41 Chronic graft-versus-host disease (cGVHD) is a notorious complication

42 Chronic graft-versus-host disease (cGVHD) is a serious complication of

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

44 Chronic graft-versus-host disease (cGVHD) is associated with inadequat

45 s in the pathogenesis of cGVHD.Chronic graft-versus-host disease (cGVHD) is mediated by specific CD4

46 Chronic graft-versus-host disease (cGVHD) is the main cause of late no

47 Although chronic graft-versus-host disease (CGVHD) is the primary nonrelapse co

48 Chronic graft-versus-host disease (cGVHD) remains a major complication

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

50 Chronic graft-versus-host disease (cGVHD) remains one of the most sign

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

52 te globulin-Fresenius) reduces chronic graft-versus-host disease (cGVHD) without compromising surviva

53 contribute to pathogenesis in chronic graft-versus-host disease (cGVHD), a condition manifested by b

54 transplantation is hampered by chronic graft-versus-host disease (cGVHD), resulting in multiorgan fib

55 athological role of B cells in chronic graft-versus-host disease (cGVHD).

56 peutic effect in patients with chronic graft-versus-host disease (cGvHD).

57 A history of graft-versus-host disease (GVHD) ( n = 27) was associated with

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

59 e cumulative incidence (CI) of chronic graft-versus-host disease (GvHD) (hazards ratio [HR], 0.4; 95%

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

61 e therapy required to prevent or treat graft-versus-host disease (GVHD) after allogeneic blood or mar

62 cells (Tregs) can control experimental graft-versus-host disease (GVHD) after allogeneic hematopoieti

63 s) associated with the risk of chronic graft-versus-host disease (GVHD) after allogeneic hematopoieti

64 ulatory T cells (T reg cells) suppress graft-versus-host disease (GvHD) after allogeneic hematopoieti

65 microangiopathy to steroid-refractory graft-versus-host disease (GVHD) after allogeneic stem-cell tr

66 th 8 (26%) deaths related to new-onset graft-versus-host disease (GVHD) after anti-PD-1.

67 ance immune reconstitution and prevent graft-versus-host disease (GVHD) after hematopoietic stem cell

68 and results in low incidence of acute graft-versus-host disease (GVHD) after reduced-intensity condi

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

70 or cause of morbidity and mortality in graft-versus-host disease (GVHD) and is attributable to T cell

71 significant complications, principally graft-versus-host disease (GVHD) and opportunistic infections.

72 Graft-versus-host disease (GVHD) and posttransplant immunodefi

73 egies are used to mitigate the risk of graft-versus-host disease (GvHD) and rejection associated with

74 However, graft-versus-host disease (GVHD) and relapse after allo-HSCT r

75 reduced incidence and delayed onset of graft-versus-host disease (GVHD) and significantly prolonged s

76 le of TNF and intestinal cell death in graft-versus-host disease (GVHD) and the ability of TWEAK to e

77 health and predicts reduced intestinal graft-versus-host disease (GVHD) and treatment-related mortali

78 donor T cells caused less severe acute graft-versus-host disease (GVHD) and yielded higher numbers of

79 hat donor effector T-cell function and graft-versus-host disease (GVHD) are regulated via recipient i

80 odel of acute and chronic (lupus-like) graft-versus-host disease (GVHD) as models of a CTL-mediated o

81 after RIC, we hypothesize that higher graft-versus-host disease (GVHD) associated with PB transplant

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

83 be critical for CD8(+) T cell-mediated graft-versus-host disease (GVHD) but dispensable for GVHD medi

84 omes in patients with gastrointestinal graft-versus-host disease (GVHD) by measuring 23 biomarkers in

85 lls (TEM) are less capable of inducing graft-versus-host disease (GVHD) compared with naive T cells (

86 ne reconstitution and if any resultant graft-versus-host disease (GVHD) could be controlled by admini

87 mulation resulting in severe pulmonary graft-versus-host disease (GVHD) following allogeneic hematopo

88 gets for the therapy and prevention of graft-versus-host disease (GVHD) following allogeneic hematopo

89 ransplant recipients experienced acute graft-versus-host disease (GVHD) following aNK-DLI, with grade

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

91 Acute graft-versus-host disease (GVHD) grades 2-4 was more frequent

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

93 so mediated accelerated onset of acute graft-versus-host disease (GVHD) in a murine model, characteri

94 Azacitidine (AzaC) mitigates graft-versus-host disease (GvHD) in both murine preclinical tr

95 king strategy can increase the risk of graft-versus-host disease (GVHD) in murine models.

96 have been associated with an increased graft-versus-host disease (GVHD) incidence, and the MICA-129 (

97 The development of graft-versus-host disease (GVHD) is a common complication of t

98 Graft-versus-host disease (GVHD) is a complication of allogene

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

100 Sclerotic graft-versus-host disease (GVHD) is a distinctive phenotype of

101 Acute graft-versus-host disease (GvHD) is a life-threatening complic

102 Graft-versus-host disease (GvHD) is a life-threatening immunol

103 Graft-versus-host disease (GVHD) is a major cause of morbidity

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

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

106 atologic malignancies, but the risk of graft-versus-host disease (GVHD) is a major limitation for wid

107 Graft-versus-host disease (GVHD) is a severe complication of h

108 Graft-versus-host disease (GVHD) is common after allogeneic he

109 The risk of acute graft-versus-host disease (GVHD) is higher after allogeneic he

110 However, graft-versus-host disease (GVHD) is mediated by the same T cel

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

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

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

114 Graft-versus-host disease (GVHD) is the major cause of nonrela

115 Graft-versus-host disease (GVHD) is the major limitation of al

116 Lower gastrointestinal (GI) tract graft-versus-host disease (GVHD) is the predominant cause of m

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

118 diation exposure during transplant and graft-versus-host disease (GVHD) may increase risk of later ma

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

120 e encouragement that important chronic graft-versus-host disease (GVHD) patient outcomes (such as ove

121 s tacrolimus/methotrexate (Tac/Mtx) as graft-versus-host disease (GVHD) prophylaxis after matched-rel

122 transplant cyclophosphamide (PT-Cy) as graft-versus-host disease (GVHD) prophylaxis has revolutionize

123 Graft-versus-host disease (GVHD) prophylaxis included calcineu

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

125 posttransplant cyclophosphamide-based graft-versus-host disease (GVHD) prophylaxis, whereas URD reci

126 posttransplant cyclophosphamide-based graft-versus-host disease (GVHD) prophylaxis.

127 ell transplantation (HSCT) and enteric graft-versus-host disease (GVHD) remain unexplored.

128 Chronic graft-versus-host disease (GVHD) remains a common and potentia

129 ation continue to improve, but chronic graft-versus-host disease (GVHD) remains a common toxicity and

130 espite major advances in recent years, graft-versus-host disease (GVHD) remains a major life-threaten

131 Intestinal graft-versus-host disease (GVHD) remains a significant obstacl

132 Treatment of steroid-resistant acute graft-versus-host disease (GVHD) remains an unmet clinical nee

133 presented to donor T cells to generate graft-versus-host disease (GVHD) represents an attractive ther

134 Graft-versus-host disease (GVHD) represents the major nonrelap

135 itutes of Health (NIH)-defined chronic graft-versus-host disease (GVHD) requiring systemic treatment

136 We show that B7-H3 is upregulated in graft-versus-host disease (GVHD) target organs, including the

137 e of T cells during breakthrough acute graft-versus-host disease (GVHD) that occurs in the setting of

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

139 third-party mice protects from lethal graft-versus-host disease (GVHD) through expansion of donor re

140 amin A levels would reduce the risk of graft-versus-host disease (GVHD) through reduced gastrointesti

141 Overall incidences of graft-versus-host disease (GVHD) were similar, but chronic GVH

142 have been shown to effectively prevent graft-versus-host disease (GVHD) when adoptively transferred i

143 gnize host tissues as foreign, causing graft-versus-host disease (GVHD) which is a main contributor t

144 ll transplantation (HSCT), controlling graft-versus-host disease (GVHD) while maintaining graft-versu

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

146 trials of initial treatment of chronic graft-versus-host disease (GVHD), and evidence showing the ass

147 ransplantation (allo-HCT) are relapse, graft-versus-host disease (GVHD), and infection.

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

149 s a strategy to reduce the severity of graft-versus-host disease (GVHD), and recalibrate the effector

150 hich led respectively to rejection and graft-versus-host disease (GVHD), being overcome through trans

151 orrected cells would avoid the risk of graft-versus-host disease (GVHD), but the genotoxicity of cond

152 kade of PD-1 increases the severity of graft-versus-host disease (GVHD), but the interplay between PD

153 d understanding of histocompatibility, graft-versus-host disease (GVHD), GVL effect, and immune recon

154 A) can mediate late immunopathology in graft-versus-host disease (GVHD), however protective roles rem

155 Complications include graft failure, graft-versus-host disease (GVHD), infection, and transplant-re

156 as individual complications, including graft-versus-host disease (GVHD), relapse, or death, yet no on

157 thogenesis of intestinal mucositis and graft-versus-host disease (GVHD), these cytokines are consider

158 patients developing acute and chronic graft-versus-host disease (GVHD), we reasoned that inhibition

159 en shown to exacerbate the severity of graft-versus-host disease (GVHD), whereas costimulation of CD8

160 the driving force in the induction of graft-versus-host disease (GVHD), yet little is known about T

161 SCT), using the composite end point of graft-versus-host disease (GVHD)-free and progression-free sur

162 ypersensitivity (CHS) and experimental graft-versus-host disease (GVHD)-like disease.

163 tween groups in the incidence of acute graft-versus-host disease (GVHD).

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

165 f inflammatory bowel disease and acute graft-versus-host disease (GVHD).

166 e healthy tissues resulting in harmful graft-versus-host disease (GVHD).

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

168 arget tissues reduces the incidence of graft-versus-host disease (GVHD).

169 emia but have the potential to mediate graft-versus-host disease (GVHD).

170 the subsequent development of chronic graft-versus-host disease (GVHD).

171 ty in inflammatory diseases, including graft-versus-host disease (GVHD).

172 D-1H agonistic mAb protected mice from graft-versus-host disease (GVHD).

173 ntation (allo-HCT) is limited by acute graft-versus-host disease (GVHD).

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

175 ut carries a significant risk of acute graft-versus-host disease (GVHD).

176 potentially lethal inflammation called graft-versus-host disease (GVHD).

177 tiate between relapse and the onset of graft-versus-host disease (GVHD).

178 ng infections and an increased risk of graft-versus-host disease (GVHD).

179 ause of impaired antiviral immunity in graft-versus-host disease (GVHD).

180 creased mortality and gastrointestinal graft-versus-host disease (GVHD).

181 ell transplantation resulting in acute graft-versus-host disease (GVHD).

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

183 e associated with an increased risk of graft-versus-host disease (GVHD).

184 sed for preventing graft rejection and graft-versus-host disease (GVHD); no patient received any post

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

186 , 2.14; 95% CI, 1.88-2.45) and without graft-versus-host disease (odds ratio, 1.35; 95% CI, 1.19-1.54

187 c stem cell transplant recipients with graft-versus-host disease (odds ratio, 2.14; 95% CI, 1.88-2.45

188 0.004, hazard ratio = 8.2) and chronic graft-versus-host disease (P = 0.010, hazard ratio = 5.3) were

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

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

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

192 Transfusion-associated graft-versus-host disease (TA-GVHD) is a rare complication of

193 icity (veno-occlusive disease or acute graft versus-host disease [GvHD]); chronic GvHD; overall survi

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

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

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

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

198 roduced to the conditioning to prevent graft-versus-host disease and graft failure, negatively influe

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

200 agnosis and evaluation of treatment of graft-versus-host disease and holds promise for other diseases

201 .5 months, two of 10 (20%) died due to graft-versus-host disease and infection, respectively.

202 cal 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, establishing or

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

205 udies demonstrating Tregs can decrease graft-versus-host disease and vasculitides, there is considera

206 t CMV infection as long as they had no graft-versus-host disease and/or were not receiving systemic c

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

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

209 ctive in preventing the development of graft-versus-host disease compared with polyclonal Tregs.

210 ias) was reported in 4 patients, acute graft-versus-host disease grade 1 in 2, grade 2 in 3, and grad

211 atients who developed acute or chronic graft-versus-host disease had a longer overall survival (OS; P

212 No treatment-related death or graft-versus-host disease had been reported; 15 of the 17 pati

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

214 The CI of acute graft-versus-host disease II to IV was 32.3% after RIC and 37.

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

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

217 lls in association with clinical acute graft-versus-host disease in allogeneic hematopoietic cell tra

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

219 tion with OVA and induction of chronic graft-versus-host disease in female ERalpha-knockout mice.

220 Four patients had graft-versus-host disease in the 45 days after VST infusion, w

221 s observed, except for a grade II skin graft-versus-host disease in the patient treated for hematolog

222 ted mortality (TRM), acute and chronic graft-versus-host disease incidence and severity, time to engr

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

224 Ngamma-secreting Tregs in a xenogeneic graft-versus-host disease model and in adoptive transfer model

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

226 indings were confirmed in T-cells from graft-versus-host disease patients treated with extracorporeal

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

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

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

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

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

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

233 erexpression of IFN-inducible genes in graft-versus-host disease skin and markedly reduced dermal IFN

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

235 ive 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% after

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

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

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

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

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

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

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

244 ell responses during organ transplant, graft-versus-host disease, and allergies are also major clinic

245 g patients receiving HCT, 27 (40%) had graft-versus-host disease, and most deaths occurred within 1 y

246 e cortisone-resistant gastrointestinal graft-versus-host disease, and the patient died from multiple

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

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

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

250 ed by acid reflux, allergic responses, graft-versus-host disease, drugs, or infections, is a common c

251 val, 1.84-31.7), controlling for acute graft-versus-host disease, in 109 patients with Philadelphia-c

252 rejection without inducing xenogeneic graft-versus-host disease, thus resulting in significantly hig

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

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

255 riteria for Clinical Trials in Chronic Graft-Versus-Host Disease.

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

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

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

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

260 use model of TCR gene transfer-induced graft-versus-host disease.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

278 ute toxicities or significant onset of graft-versus-host disease.

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

280 lammatory bowel disease and allogeneic graft-versus-host disease.

281 mens, corticosteroids, infections, and graft-versus-host disease.

282 counting for immune reconstitution and graft-versus-host disease.

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

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

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

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

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

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

289 erocolitis resembling acute intestinal graft-versus-host-disease.

290 ntitumour immunity and pathogenesis of graft-versus-host diseases.

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

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

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

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

295 nvironment has critical effects on the graft-versus-host (GVH) responses mediated by naive donor T ce

296 retina cells represents a mechanism of graft-versus-host interaction following hematopoietic cell tra

297 LT mice that spontaneously developed a graft-versus-host-like condition, characterized by alopecia an

298 The graft-versus-host reaction of CD4(+) T cells, but not of CD8(+

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

300 tured with this process do not mediate graft-versus-host reactions and are rendered resistant to dest