ライフサイエンスコーパス: versus host

1 eroid-dependent or -refractory chronic graft-versus-host diesease (cGVHD) are poor, and only ibrutini

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

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

4 s, including organ transplantation and graft versus host disease (GVHD) but they have limitations.

5 ting prevention strategies for chronic graft versus host disease (GVHD) have measured its cumulative

6 Severe pulmonary chronic graft versus host disease (GVHD) is a life-threatening complic

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

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

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

10 ts expired by day 40 from severe acute graft versus host disease (GVHD).

11 ity and mortality rates, mainly due to graft versus host disease (GvHD).

12 ycine (DMOG) in the pathophysiology of graft versus host disease (GVHD).

13 oproliferative disorder (P = 0.09) and graft versus host disease (P = 0.002).

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

15 n and treatments for acute and chronic graft versus host disease after transplantation.

16 or its occurrence were the presence of graft versus host disease and the use of alemtuzumab.

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

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

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

20 ction or consolidation chemotherapy or graft versus host disease treatment in hematopoietic stem cell

21 te antiglobulin, and acute and chronic graft versus host disease were significantly associated with p

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

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

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

25 s who develop steroid-refractory acute graft-versus-host disease (aGVHD) after allogeneic hematopoiet

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

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

28 Acute graft-versus-host disease (aGVHD) hinders the efficacy of allo

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

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

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

32 severe and/or steroid-refractory acute graft-versus-host disease (aGVHD) remains a significant limita

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

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

35 ral reactivation, grade II to IV acute graft-versus-host disease (aGvHD), and chronic graft-versus-ho

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

37 nnected to a higher incidence of acute graft-versus-host disease (aGVHD).

38 5.55; P = 0.002) and grade II-IV acute graft-versus-host disease (aHR, 1.59; 95% CI, 1.06-2.39; P = 0

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

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

41 y attributable to experimental chronic graft-versus-host disease (cGVHD) by targeting B-cell lymphoma

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

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

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

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

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

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

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

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

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

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

52 Chronic graft-versus-host disease (cGVHD) represents a double-edged sw

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

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

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

56 lications in a murine model of chronic graft-versus-host disease (cGVHD).

57 oimmune-like syndrome known as chronic graft-versus-host disease (cGVHD).

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

59 Chronic pulmonary graft-versus-host disease (cpGVHD) after hematopoietic cell tr

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

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

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

63 Graft-versus-host disease (GVHD) after allogeneic stem cell tr

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

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

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

67 e-threatening complications, including graft-versus-host disease (GVHD) and infections, which are fac

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

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

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

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

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

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

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

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

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

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

78 ontributed to significant reduction in graft-versus-host disease (GVHD) but retained sufficient graft

79 ny-stimulating factor (GM-CSF) promote graft-versus-host disease (GVHD) by recruiting donor dendritic

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

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

82 nt is development of acute xenogeneic graft- versus-host disease (GVHD) due to human T-cell recogniti

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

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

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

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

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

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

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

90 Graft-versus-host disease (GVHD) in the gastrointestinal (GI)

91 We have shown that under acute graft-versus-host disease (GVHD) inflammatory conditions, RA i

92 Graft-versus-host disease (GvHD) is a common complication of h

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

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

95 Acute graft-versus-host disease (GVHD) is a frequent complication of

96 Intestinal graft-versus-host disease (GVHD) is a life-threatening complic

97 Acute graft-versus-host disease (GVHD) is a life-threatening complic

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

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

100 Chronic graft-versus-host disease (GVHD) is a major complication of al

101 Graft-versus-host disease (GvHD) is a major complication of al

102 Graft-versus-host disease (GVHD) is a major factor contributin

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

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

105 Acute graft-versus-host disease (GVHD) is initially triggered by all

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

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

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

109 Graft-versus-host disease (GVHD) is the most serious complicat

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

111 our understanding of how PTCy prevents graft-versus-host disease (GVHD) largely has been extrapolated

112 pointing to exacerbation of underlying graft-versus-host disease (GVHD) linked to presence of human T

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

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

115 Gastrointestinal acute graft-versus-host disease (GVHD) occurring after allogeneic he

116 r the patient has or has not developed graft-versus-host disease (GvHD) or received immunosuppressant

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

118 tools may identify a lower-risk acute graft-versus-host disease (GVHD) population amenable to novel,

119 Graft-versus-host disease (GvHD) presents a major cause for mo

120 Despite graft-versus-host disease (GVHD) prophylactic agents, the succ

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

122 P) and mycophenolate mofetil (MMF) for graft-versus-host disease (GVHD) prophylaxis after nonmyeloabl

123 e tacrolimus and sirolimus (T/S)-based graft-versus-host disease (GvHD) prophylaxis has been effectiv

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

125 as represented the standard of care in graft-versus-host disease (GVHD) prophylaxis in patients under

126 plantation from haploidentical donors; graft-versus-host disease (GVHD) prophylaxis included post-HCT

127 ed post-transplant cyclophosphamide as graft-versus-host disease (GVHD) prophylaxis to expand donor o

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

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

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

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

132 Acute graft-versus-host disease (GVHD) remains a major limitation of

133 Graft-versus-host disease (GVHD) remains a major limitation of

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

135 Graft-versus-host disease (GVHD) remains an important cause of

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

137 Graft-versus-host disease (GVHD) remains one of the major comp

138 driven by the premise that persistent graft-versus-host disease (GVHD) results from inadequate immun

139 curacy of cGVHD and to better classify graft-versus-host disease (GVHD) syndromes but have not been v

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

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

142 Prevention of graft-versus-host disease (GvHD) without malignant relapse is

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

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

145 e mortality, and severe (grade 3 or 4) graft-versus-host disease (GVHD), all evaluated through 100 da

146 ding inflammatory bowel disease (IBD), graft-versus-host disease (GVHD), and cancer.

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

148 ssion-free survival, acute and chronic graft-versus-host disease (GVHD), and GVHD-free and relapse-fr

149 logic mismatch can also lead to lethal graft-versus-host disease (GVHD), and immunosuppression strate

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

151 se of morbidity and mortality in acute graft-versus-host disease (GVHD), and pathological damage is l

152 ciated with a high risk of graft loss, graft-versus-host disease (GvHD), and transplant-related morta

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

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

155 Graft-versus-host disease (GVHD), however, remains one of the

156 ions are elevated in steroid-resistant graft-versus-host disease (GVHD), implying endothelial hypofun

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

158 no impact of EBV reactivation on acute graft-versus-host disease (GVHD), nonrelapse mortality, progre

159 bserved in a mouse model of intestinal graft-versus-host disease (GVHD), providing a roadmap for prec

160 eneic immune-mediated gastrointestinal graft-versus-host disease (GVHD), the principal toxicity after

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

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

163 ll transplantation (HCT) is limited by graft-versus-host disease (GVHD), which is the main post-trans

164 crobiome-dependent metabolite, worsens graft-versus-host disease (GVHD).

165 + graft depletion effectively prevents graft-versus-host disease (GVHD).

166 ve immunosuppression to better control graft-versus-host disease (GvHD).

167 icity of preconditioning therapies and graft-versus-host disease (GVHD).

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

169 erve damage in a mouse model of ocular graft-versus-host disease (GVHD).

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

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

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

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

174 o-immune responses will lead to lethal graft-versus-host disease (GVHD).

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

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

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

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

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

180 butes to pathology in animal models of graft-versus-host disease (GVHD).

181 kb signaling as a means of controlling graft-versus-host disease (GVHD).

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

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

184 ons, predominantly infection and acute graft-versus-host disease (GVHD).

185 al malignancies but remains limited by graft-versus-host disease (GVHD).

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

187 us-host disease (cGVHD) and late acute graft-versus-host disease (L-aGVHD) are understudied complicat

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

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

190 0.004, hazard ratio = 8.2) and chronic graft-versus-host disease (P = 0.010, hazard ratio = 5.3) were

191 tensity conditioning (P = 0.02), acute graft-versus-host disease (P = 0.03), and chronic graft-versus

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

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

194 -resistant or steroid-refractory acute graft-versus-host disease (SR-aGVHD) poses one of the most vex

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

196 ltransferase gene in T cells mediating graft-versus-host disease after allogeneic bone marrow transpl

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

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

199 s to alleviate autoimmune diseases and graft-versus-host disease after hematopoietic stem cell transf

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

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

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

203 CAR T cells may cause life-threatening graft-versus-host disease and may be rapidly eliminated by the

204 cal symptoms in animal models of acute graft-versus-host disease and multiple sclerosis.

205 is associated with low rates of severe graft-versus-host disease and nonrelapse mortality and does no

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

207 ed after transplant in the presence of graft-versus-host disease and were not replaced, owing to poor

208 ation without steroid-refractory acute graft-versus-host disease and without early relapse.

209 This study also supports chronic graft-versus-host disease as a risk factor for nonmelanoma ski

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

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

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

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

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

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

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

217 ing T cell regeneration and mitigating graft-versus-host disease in HSCT.

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

219 ght patients (38%), grade 1 acute skin graft-versus-host disease in two patients (10%), and grade 4 p

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

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

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

223 iver-thymus (BLT) mouse model prone to graft-versus-host disease occurred only following reversion of

224 ipients without increasing the risk of graft-versus-host disease or disease relapse.

225 cyclophosphamide, and fludarabine) and graft-versus-host disease prophylaxis (calcineurin inhibitor a

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

227 t unrelated donors, using conventional graft-versus-host disease prophylaxis.

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

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

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

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

232 ceiving systemic immunosuppression for graft-versus-host disease treatment.

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

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

235 In multivariate analysis, chronic graft-versus-host disease was a significant risk factor for dr

236 Worsening graft-versus-host disease was not identified among Allo recipi

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

238 ount <300 cells/uL at D +30, and acute graft-versus-host disease were predictors of ADV viremia in mu

239 sociated with morbidity, rejection and graft-versus-host disease(2).

240 panied by morbidity and mortality from graft-versus-host disease(5).

241 ding hepatitis B virus infection(5-7), graft-versus-host disease(8) and inflammatory bowel disease(9,

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

243 ansplant lymphoproliferative disorder, graft-versus-host disease, and enteric infections.

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

245 sive mold infection, acute and chronic graft-versus-host disease, and prednisone exposure.

246 ne release syndrome, neurotoxicity, or graft-versus-host disease, and there was no increase in the le

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

248 Lack of acute xenogeneic graft- versus-host disease, but retention of T-cell function fo

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

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

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

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

253 ammatory episodes, or acute or chronic graft-versus-host disease, occurred in any patient.

254 ng patients who developed severe acute graft-versus-host disease, suggesting that short telomere leng

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

256 lead to inflammatory disorders such as graft-versus-host disease, transplant rejection and autoimmune

257 itions such as hepatitis C vasculitis, graft-versus-host disease, type 1 diabetes, and systemic lupus

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

259 tients were alive, without evidence of graft-versus-host disease, with major infection at 1 year in o

260 was shown to predict death after acute graft-versus-host disease.

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

262 acterial infection, colitis, and acute graft-versus-host disease.

263 me-like phenotype and aggravated acute graft-versus-host disease.

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

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

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

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

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

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

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

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

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

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

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

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

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

277 reduced survival and increased chronic graft-versus-host disease.

278 une diseases, transplant rejection and graft-versus-host disease.

279 CD43 in multiple T cell subsets during graft-versus-host disease.

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

281 ssue manifestations of T-cell-mediated graft-versus-host disease.

282 might promote graft immunogenicity or graft-versus-host disease.

283 intensive care unit admissions; acute graft-versus-host disease; Bearman toxicity score; sinusoidal

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

285 transplantation; steroid use, chronic graft-versus-host disease; use of fludarabine, melphalan, and

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

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

288 apy reported substantial toxicity from graft-versus-host-disease (GVHD).

289 lent graft function after overcoming a graft-versus-host-disease episode 5 months posttransplant.

290 hnicity, malignant disease, graft, and graft-versus-host-disease prophylaxis), ST2 remained associate

291 fibrosis and show promising results in graft-versus-host-disease.

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

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

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

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

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

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

298 rupting agents that selectively target virus versus host membranes could potentially inhibit a broad-

299 ma, allowing the complex dissection of tumor versus host pathogenic seizure mechanisms.

300 tical sources of Delta-like ligands in graft-versus-host responses irrespective of conditioning inten