ライフサイエンスコーパス: GVHD

1 GVHD increased microglia TGF-beta-activated kinase-1 (TA

2 GVHD is initiated by the interaction between recipient a

3 GVHD manifestations that persist without improvement in

4 GVHD prophylaxis comprised cyclosporine, mycophenolate m

5 GVHD was observed in 8.8% (39/445); median time-to-GVHD

6 D, including four (24%) with maximal grade 2 GVHD and one (6%) with grade 3 GVHD.

7 ximal grade 2 GVHD and one (6%) with grade 3 GVHD.

8 tly limits the occurrence of acute grade 2-4 GVHD after reduced intensity conditioning PBSC h-HSCT, p

9 Three patients developed grade 2 to 4 GVHD.

10 e activated by donor monocytes to generate a GVHD-like dermatitis.

11 Acute GVHD was induced in lethally irradiated BALB/c mice.

12 id doses for the management of grade 2 acute GVHD with isolated skin or upper gastrointestinal tract

13 gle HLA-B mismatch increased grade 3-4 acute GVHD (odds ratio [OR] 1.89, 95% CI 1.53-2.33; p<0.0001).

14 the cumulative incidence of grade 2-4 acute GVHD at day 100 post-transplantation.

15 e cumulative incidence of grade 2 to 4 acute GVHD at day 100 was 36% (95% confidence interval [CI], 2

16 The cumulative incidence of grade 2-4 acute GVHD at day 100 was lower in the triple-drug group compa

17 e cumulative incidence of grade 2 to 4 acute GVHD could be reduced to <70% in HLA class I or II misma

18 9%) of 17 patients developed grade 2-4 acute GVHD, including four (24%) with maximal grade 2 GVHD and

19 lective inhibitor, GNF362, ameliorated acute GVHD without impairing GVL against 2 acute myeloid leuke

20 -deleted (Itpkb-/-) T cells attenuated acute GVHD in 2 models without eliminating A20-luciferase B-ce

21 lls were present in all skin and colon acute GVHD specimens studied, yet were largely absent in blood

22 In conclusion, acute GVHD damages and prevents repair of the FRC network, thu

23 A dose-dependent acute GVHD process was observed with progressive weight loss,

24 ower proportion of patients developing acute GVHD compared with patients treated with cyclosporine an

25 Itpkb signaling is essential to drive acute GVHD pathogenesis and sustain active chronic GVHD, point

26 patient skin, colon, and blood during acute GVHD.

27 e implanted in RRGS animals and elicit acute GVHD or rejection of human tumor cells and these are use

28 pared with FK506, GNF362 had favorable acute GVHD and GVL properties against MLL-AF9-eGFP cells.

29 r addition of new systemic therapy for acute GVHD, 0.46; 95% CI, 0.35 to 0.60).

30 t have a pathophysiology distinct from acute GVHD, Itpkb-/- donor T cells reduced active chronic GVHD

31 clear cells (hPBMCs) to set up a human acute GVHD model.

32 n-presenting cells (APCs) in tissue in acute GVHD were donor derived, and donor-derived APCs were obs

33 To evaluate the role of TIPE in acute GVHD, naive C57BL/6 and Tipe C57BL/6 mice were condition

34 ously unappreciated pathogenic role in acute GVHD.

35 files in chronic GVHD (cGVHD) and late acute GVHD (L-aGVHD).

36 tivation in vivo, we established a new acute GVHD model mediated by clonal alloantigen-specific 4C CD

37 agonist, teduglutide, reduced de novo acute GVHD and steroid-refractory GVHD, without compromising g

38 evidence for alternative mechanisms of acute GVHD (aGVHD) in humans.

39 The cumulative incidence of acute GVHD grade 2 to 4 was 0.17 in the MUD group and 0.22 in

40 hs) with the typical manifestations of acute GVHD involving the skin, liver, and intestines.

41 GVHD and that GLP-2-based treatment of acute GVHD restores intestinal homeostasis via an increase of

42 resh insights into the pathogenesis of acute GVHD, and translation of these insights toward developme

43 fetil resulted in a lower incidence of acute GVHD, thus translating into superior overall survival co

44 Is, in the prevention and treatment of acute GVHD.

45 Past acute GVHD and peripheral blood grafts are major risk factors

46 m (L1S1) antibody completely prevented acute GVHD.

47 til prophylaxis therapy for preventing acute GVHD in this setting.

48 lder who had glucocorticoid-refractory acute GVHD after allogeneic stem-cell transplantation.

49 opose to define ruxolitinib-refractory acute GVHD as disease that shows: (1) progression of GVHD comp

50 treatment of corticosteroid-refractory acute GVHD in adult and pediatric patients 12 years and older.

51 es were detected in steroid-refractory acute GVHD, disease-free survival, relapse, nonrelapse mortali

52 atients with glucocorticoid-refractory acute GVHD.

53 atients with corticosteroid-refractory acute GVHD.

54 Incidence of severe acute GVHD after injection was similar between groups (hazard

55 Only half of patients with severe acute GVHD respond to first-line treatment with corticosteroid

56 with clinical- and biomarker-based SR acute GVHD, sirolimus demonstrates similar overall initial tre

57 nt of patients with standard risk (SR) acute GVHD as defined by the Minnesota (MN) GVHD Risk Score an

58 Here, we tested the hypothesis that acute GVHD blocks peripheral tolerance of autoreactive T cells

59 We observed that acute GVHD reduced intestinal GLP-2 levels in mice and patient

60 gle HLA-B-mismatched transplantations, acute GVHD risk was higher with leader mismatching than with l

61 vide a TAK1 inhibitor-based approach against GVHD-induced neurotoxicity.

62 ncluding immunodepression, autoimmunity, and GVHD might be intensified by injury.

63 s group, the most common being infection and GVHD.

64 Mortality and GVHD increased with increasing numbers of HLA mismatches

65 ents, but pre-HSCT conditioning regimens and GVHD create a challenging inflammatory environment for T

66 yl + PTCY (n = 32) or PTCY + ATG (n = 26) as GVHD prophylaxis.

67 By using post-transplant cyclophosphamide as GVHD prophylaxis, we successfully expanded alloBMT donor

68 ndicate that Sirt-1 inhibition can attenuate GVHD while preserving the graft-versus-leukemia effect.

69 emains unknown whether Notch blockade blunts GVHD through its effects on Tconv, Tregs, or both and wh

70 the mucosal barrier mucosa is compromised by GVHD.

71 ll transplantation (allo-HSCT) is limited by GVHD.

72 Chronic GVHD developed in three (18%) patients.

73 tpkb-/- donor T cells reduced active chronic GVHD in a multiorgan system model of bronchiolitis oblit

74 GNF362 treatment reduced active chronic GVHD in both BO and scleroderma models.

75 GVHD pathogenesis and sustain active chronic GVHD, pointing toward a novel clinical application to pr

76 mulative incidence at 2 years of all chronic GVHD was 40%, and moderate/severe chronic GVHD was 10%.

77 s-host disease (GVHD) in 9 (6%), and chronic GVHD in 23 (12%).

78 erapy to prevent and treat acute and chronic GVHD, in the context of GVHD pathophysiology.

79 isted following EBV reactivation and chronic GVHD, with a reciprocal decrease in NKG2C subset, wherea

80 nagement, and treatment of acute and chronic GVHD.

81 s for resteroid-refractory acute and chronic GVHD.

82 sed in the target organs affected by chronic GVHD.

83 pe (WT) APC to mice with established chronic GVHD (cGVHD), a less-inflammatory autoimmune-like diseas

84 32) evaluated the immune profiles in chronic GVHD (cGVHD) and late acute GVHD (L-aGVHD).

85 there was a significant increase in chronic GVHD following EBV reactivation (62.5% versus 8%; P = 0.

86 In chronic GVHD preclinical models that have a pathophysiology dist

87 hich might have a pathogenic role in chronic GVHD.

88 The cumulative incidence of chronic GVHD at 24 months was 26.3% (95% CI 17.5-35.1) in the an

89 Symptoms of chronic GVHD by the Lee Scale were more prevalent in the standar

90 sed within 3 months of subsidence of chronic GVHD.

91 ic GVHD was 40%, and moderate/severe chronic GVHD was 10%.

92 in use of immunosuppressive therapy, chronic GVHD and its symptoms, depressive symptoms, and improved

93 Subsequent transition to chronic GVHD involves the emergence of autoimmunity, although th

94 pplication to prevent acute or treat chronic GVHD.

95 inical features more consistent with chronic GVHD (cGVHD) are lacking, raising concern of underrecogn

96 relationship of the microbiome with chronic GVHD (cGVHD) by analyzing stool and plasma samples colle

97 verse was witnessed in those without chronic GVHD (P < 0.01).

98 Animals were monitored for clinical GVHD and analyzed at day +7 and at day +50.

99 : 85% versus 37%; P < 0.05), higher clinical GVHD scores, more profound weight loss, increased serum

100 The role of microglia in CNS-GVHD remains undefined.

101 ummary, we prove a role for microglia in CNS-GVHD, identify the TAK1/TNF/MHC-II axis as a mediator of

102 he TAK1/TNF/MHC-II axis as a mediator of CNS-GVHD, and provide a TAK1 inhibitor-based approach agains

103 rified microglia obtained from mice with CNS-GVHD revealed TNF upregulation.

104 single-cell suspensions from acute cutaneous GVHD and subjected them to genotype, transcriptome, and

105 e gp130Fc promoted severe, chronic cutaneous GVHD.

106 For decades, GVHD prophylaxis has included calcineurin inhibitors, de

107 intaining classical IL-6 signaling-dependent GVHD responses.

108 Mice that went on to develop GVHD showed signs of rapid proliferation in the human T

109 itrated doses of human bone marrow developed GVHD that was characterized by widespread lymphocyte inf

110 GLP-2 levels in mice and patients developing GVHD.

111 ations, including graft-versus-host disease (GVHD) and infections, which are factors limiting its wid

112 s associated with graft-versus-host disease (GVHD) and mortality.

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

114 Human graft-versus-host disease (GVHD) biology beyond 3 months after hematopoietic stem c

115 cant reduction in graft-versus-host disease (GVHD) but retained sufficient graft versus tumor (GVT) r

116 ansplantation and graft versus host disease (GVHD) but they have limitations.

117 (GM-CSF) promote graft-versus-host disease (GVHD) by recruiting donor dendritic cells.

118 Acute graft-versus-host disease (GVHD) can affect the central nervous system (CNS).

119 acute xenogeneic graft- versus-host disease (GVHD) due to human T-cell recognition of murine major hi

120 gher incidence of graft-versus-host disease (GVHD) has been observed after haploidentical hematopoiet

121 egies for chronic graft versus host disease (GVHD) have measured its cumulative incidence.

122 6%), severe acute graft-versus-host disease (GVHD) in 9 (6%), and chronic GVHD in 23 (12%).

123 Graft-versus-host disease (GVHD) in the gastrointestinal (GI) tract is the principa

124 Acute graft-versus-host disease (GVHD) is a frequent complication of hematopoietic transp

125 Acute graft-versus-host disease (GVHD) is a life-threatening complication after allogenei

126 pulmonary chronic graft versus host disease (GVHD) is a life-threatening complication of allogeneic h

127 Intestinal graft-versus-host disease (GVHD) is a life-threatening complication of allogeneic h

128 Graft-versus-host disease (GVHD) is a major cause of morbidity and mortality in hem

129 Chronic graft-versus-host disease (GVHD) is a major complication of allogeneic hematopoieti

130 Graft-versus-host disease (GVHD) is a major factor contributing to mortality and mo

131 Acute graft-versus-host disease (GVHD) is initially triggered by alloreactive T cells, wh

132 Graft-versus-host disease (GVHD) is the most serious complication of allogeneic hem

133 how PTCy prevents graft-versus-host disease (GVHD) largely has been extrapolated from major histocomp

134 ion of underlying graft-versus-host disease (GVHD) linked to presence of human T cells in the marrow.

135 ointestinal acute graft-versus-host disease (GVHD) occurring after allogeneic hematopoietic cell tran

136 lower-risk acute graft-versus-host disease (GVHD) population amenable to novel, reduced-intensity tr

137 Despite graft-versus-host disease (GVHD) prophylactic agents, the success and wider utiliza

138 mofetil (MMF) for graft-versus-host disease (GVHD) prophylaxis after nonmyeloablative conditioning fo

139 andard of care in graft-versus-host disease (GVHD) prophylaxis in patients undergoing a mismatched un

140 clophosphamide as graft-versus-host disease (GVHD) prophylaxis to expand donor options and an optimis

141 Graft-versus-host disease (GVHD) remains a major limitation of allogeneic hematopoi

142 Acute graft-versus-host disease (GVHD) remains a major limitation of allogeneic stem-cell

143 Acute graft-versus-host disease (GVHD) remains a major obstacle for the wider usage of al

144 Graft-versus-host disease (GVHD) remains an important cause of morbidity and mortal

145 e that persistent graft-versus-host disease (GVHD) results from inadequate immunosuppression.

146 Graft-versus-host disease (GVHD), a common complication after peripheral blood stem

147 re (grade 3 or 4) graft-versus-host disease (GVHD), all evaluated through 100 days after HCT, and gra

148 el disease (IBD), graft-versus-host disease (GVHD), and cancer.

149 ortality in acute graft-versus-host disease (GVHD), and pathological damage is largely attributable t

150 Graft-versus-host disease (GVHD), however, remains one of the most potentially life

151 steroid-resistant graft-versus-host disease (GVHD), implying endothelial hypofunctioning for thrombom

152 in the absence of graft-versus-host disease (GVHD), neurotoxicity, or dose-limiting toxicities.

153 tivation on acute graft-versus-host disease (GVHD), nonrelapse mortality, progression-free, or overal

154 del of intestinal graft-versus-host disease (GVHD), providing a roadmap for precision medicine.

155 CT) is limited by graft-versus-host disease (GVHD), which is the main post-transplantation challenge

156 transplantation, graft versus host disease (GVHD), while relatively rare, remains a major cause of m

157 tabolite, worsens graft-versus-host disease (GVHD).

158 animal models of graft-versus-host disease (GVHD).

159 ns of controlling graft-versus-host disease (GVHD).

160 athophysiology of graft versus host disease (GVHD).

161 s consistent with graft-versus-host disease (GVHD).

162 fection and acute graft-versus-host disease (GVHD).

163 emains limited by graft-versus-host disease (GVHD).

164 ectively prevents graft-versus-host disease (GVHD).

165 from severe acute graft versus host disease (GVHD).

166 ll lead to lethal graft-versus-host disease (GVHD).

167 Acute graft-versus-host-disease (GVHD) after non-myeloablative human leucocyte antigen (H

168 ial toxicity from graft-versus-host-disease (GVHD).

169 is a main driver of allogeneic T cell-driven GVHD, oxidative phosphorylation is a main driver of Treg

170 entation of an intestinal PTA by FRCs during GVHD resulted in the activation of autoaggressive T cell

171 s pathological damage in the GI tract during GVHD.

172 ed neutrophil activation that promotes early GVHD and opens a new avenue to interfere with aGVHD with

173 Subsequently, they created the EBMT GVHD management recommendation expert panel by recruitin

174 occurred, including 2 irAEs and 2 with fatal GVHD.

175 the basis of T cell autoreactivity following GVHD.

176 For GVHD prophylaxis, all but 2 received serotherapy (antith

177 as the leader of the mismatched allotype for GVHD.

178 d chimeric antigen receptor (CAR) T cell for GVHD prevention.

179 Thus, the use of human CD83 CAR T cells for GVHD prevention and treatment, as well as for targeting

180 nt state of knowledge about risk factors for GVHD development following intestinal transplantation.

181 o multivariable analysis of risk factors for GVHD development has previously been reported.

182 Ideally, cellular therapy for GVHD will not affect alloreactive immune responses again

183 x model offering significant protection from GVHD development (listed in order of selection): isolate

184 itis, host NLRP6 aggravated gastrointestinal GVHD.

185 show protective effects of DMOG on early gut GVHD and improved survival in a model of allogeneic hema

186 IPE-deficient mice developed exacerbated gut GVHD compared with allo controls and had significantly d

187 ctive function during the development of gut GVHD and may be a potential future target to prevent or

188 nting 2 critical complications of allo-HCT - GVHD and relapse.

189 ies, and potential pathogenic roles of human GVHD macrophages.

190 el combination partner for immunosuppressive GVHD therapy to be tested in clinical trials.

191 In GVHD, however, there was upregulation of monocyte antige

192 nt study, we addressed the role of Sirt-1 in GVHD induction by employing Sirt-1 conditional knockout

193 valuate a potential role for host T cells in GVHD, the origin of skin and blood T cells was assessed

194 valuate the role of the leader dimorphism in GVHD after HLA-B-mismatched unrelated HCT.

195 l by recruiting 20 experts with expertise in GVHD management.

196 ic cells (DCs), which are both implicated in GVHD pathogenesis.

197 rgan involvement; (2) lack of improvement in GVHD (partial response or better) compared with baseline

198 the dominant population of all leukocytes in GVHD.

199 The HLA-B leader informs GVHD risk after HLA-B-mismatched unrelated HCT and diffe

200 re, we examined the mechanisms that initiate GVHD, including the relevant antigen-presenting cells.

201 he cellular and molecular factors initiating GVHD, both spatially and temporally, give rise to a numb

202 Interestingly, GVHD was not an inevitable outcome in our system and was

203 comes, especially including acute intestinal GVHD and reduced overall survival.

204 o the inflammatory state of acute intestinal GVHD.

205 o-SCT patients in regard to acute intestinal GVHD.

206 We found that intestinal GVHD in mice deficient in Atg16L1, an autophagy gene tha

207 Isolated GVHD macrophages stimulated greater proliferation and ac

208 e as prognostic biomarkers for risk of later GVHD development.

209 class II prevented the initiation of lethal GVHD in the GI tract.

210 alloreactive immune cells and prevent lethal GVHD in mice.

211 ell reconstitution with PTCY + ATG may limit GVHD occurrence, the quicker reconstitution of some NK c

212 lirubin levels that were attributed to liver GVHD.

213 t patients in need of a HCT, and could lower GVHD and increase availability of HCT therapy.

214 ile inhibition of T-cell autophagy mitigates GVHD without substantial loss of GVL responses.

215 mpact of host NLRP6 deficiency in mitigating GVHD was observed regardless of co-housing, antibiotic t

216 acute GVHD as defined by the Minnesota (MN) GVHD Risk Score and Ann Arbor (AA1/2) biomarker status.

217 ecially host RALDH2(+) DCs in driving murine GVHD and suggest RALDH2 inhibition or CYP26A1 induction

218 There was no GVHD-related mortality.

219 Notably, GVHD caused irreversible damage to a population of toler

220 Observed GVHD incidence was 2.4% (3/125), 0.0% (0/38), 17.9% (7/3

221 potential association between chronic ocular GVHD pathogenesis and stress-induced cellular senescence

222 factor in the development of chronic ocular GVHD, which is currently treated primarily with immunosu

223 date an additional pathway of chronic ocular GVHD.

224 g 3 days before HSCT, and (in the absence of GVHD) tapered from day 96 through to day 150.

225 daily until day 150, and (in the absence of GVHD) tapered off by day 180.

226 L through to day 150, and (in the absence of GVHD) tapered off by day 180.

227 ely in patients after HSCT in the absence of GVHD.

228 In addition, we discuss specific aspects of GVHD prophylaxis and management in the setting of haploi

229 nd TNF production of microglia in the CNS of GVHD patients.

230 at acute and chronic GVHD, in the context of GVHD pathophysiology.

231 tanding of Treg metabolism in the context of GVHD, and discusses potential therapeutic applications o

232 or T cells are central to the development of GVHD in the gut in murine models of allogeneic bone marr

233 IL-2 levels also induced the development of GVHD.

234 ngrafted mice exhibited clinical features of GVHD.

235 resulted in significantly lower incidence of GVHD in allogeneic BMT recipients.

236 or IL-23, which are both potent inducers of GVHD-induced colonic pathology, indicating that GM-CSF c

237 At the initiation of GVHD, LN fibroblastic reticular cells (FRCs) rapidly red

238 ons as a basis for the routine management of GVHD during stem-cell transplantation.

239 blished recommendations on the management of GVHD in the setting of HLA-identical sibling or unrelate

240 e of tissue damage in the pathophysiology of GVHD rationalizes the development of cells that support

241 T cell activation metrics were predictive of GVHD onset 3-6 wk before phenotypic pathology.

242 HD as disease that shows: (1) progression of GVHD compared with baseline after at least 5 to 10 days

243 ct, positioning GM-CSF as a key regulator of GVHD in the colon and a potential therapeutic target for

244 Reports of GVHD in kidney and pancreas transplant recipients almost

245 ng the 33 982 transplantations, the risks of GVHD associated with HLA-B M and T leaders were establis

246 coccus outgrowth and reduces the severity of GVHD in mice.

247 active T cells and increases the severity of GVHD.

248 Sites of GVHD included skin (N = 21), skin/gastrointestinal tract

249 f Notch in T cells at the earliest stages of GVHD.

250 ndings indicate that L cells are a target of GVHD and that GLP-2-based treatment of acute GVHD restor

251 s of Tregs in the prevention or treatment of GVHD in cancer patients.

252 Treatment of GVHD was done with a new porcine antihuman lymphocyte se

253 riability in the prevention and treatment of GVHD worldwide.

254 response, defined as objective worsening of GVHD determined by increase in stage, grade, or new orga

255 tions Working Party created 38 statements on GVHD prophylaxis, drug management, and treatment of acut

256 D 10.94) in the anti-thymocyte globulin plus GVHD prophylaxis group and 20.38 (SD 14.68) in the stand

257 .9-23.7) in the anti-thymocyte globulin plus GVHD prophylaxis group compared with 17.5 (9.9-25.1) in

258 .6-78.6) in the anti-thymocyte globulin plus GVHD prophylaxis group compared with 53.3% (42.8-62.8) i

259 patient in the anti-thymocyte globulin plus GVHD prophylaxis group died of Epstein-Barr virus hepati

260 patients in the anti-thymocyte globulin plus GVHD prophylaxis group were free from immunosuppressive

261 n as novel therapeutic strategies to prevent GVHD.

262 T cells from hematopoietic grafts to produce GVHD.

263 uction of autophagy in donor T-cell promotes GVHD, while inhibition of T-cell autophagy mitigates GVH

264 the hazard rate of developing biopsy-proven GVHD during the first 60 months posttransplant among 445

265 e with the caspase-11 signaling might reduce GVHD while preserving GVL activity.

266 cell (Teff) ratios can substantially reduce GVHD in cancer patients, but pre-HSCT conditioning regim

267 ithymocyte globulin (ATG) may help to reduce GVHD incidence.

268 elial cells RALDH1 deletion failed to reduce GVHD.

269 g the RA-catabolizing enzyme CYP26A1 reduced GVHD.

270 ed de novo acute GVHD and steroid-refractory GVHD, without compromising graft-versus-leukemia (GVL) e

271 anti-PD-1 antibody for post-alloHCT relapse, GVHD and irAEs occurred, requiring dose deescalation, wi

272 We observed acute skin GVHD in the presence of 100% host T cells.

273 s methotrexate or mycophenolate) or standard GVHD prophylaxis alone.

274 i-thymocyte globulin 4.5 mg/kg plus standard GVHD prophylaxis (cyclosporine or tacrolimus plus methot

275 triple-drug group compared with the standard GVHD prophylaxis group (26% [95% CI 17-35] in the triple

276 pared with 53.3% (42.8-62.8) in the standard GVHD prophylaxis group (adjusted hazard ratio [HR] 0.56,

277 with 18 (19%) of 97 patients in the standard GVHD prophylaxis group (adjusted odds ratio [OR] 3.49 [9

278 group and 41.3% (31.3-51.3) in the standard GVHD prophylaxis group (p=0.032).

279 n group and 14.62 (SD 12.26) in the standard GVHD prophylaxis group (p=0.034).

280 s group and 20.38 (SD 14.68) in the standard GVHD prophylaxis group (p=0.040).

281 ompared with 17.5 (9.9-25.1) in the standard GVHD prophylaxis group (p=0.73) and non-relapse mortalit

282 In the standard GVHD prophylaxis group, 15 mg/kg of mycophenolate mofeti

283 symptoms were more prominent in the standard GVHD prophylaxis group, the mean Center for Epidemiologi

284 obulin group and in 49 (51%) in the standard GVHD prophylaxis group, the most common being infection

285 ee Scale were more prevalent in the standard GVHD prophylaxis group, with scores of 13.27 (SD 10.94)

286 y meaningful benefits when added to standard GVHD prophylaxis in patients undergoing unrelated donor

287 tional treatment (n=102) along with standard GVHD prophylaxis.

288 Subsequently, GVHD led to the selective elimination of the FRC populat

289 ents and no patients were receiving systemic GVHD therapy.

290 These reports, however, demonstrate that GVHD can additionally result from peripheral host T cell

291 as observed in 8.8% (39/445); median time-to-GVHD development (range) was 1.5 months (0.5-17.3 mo) po

292 regs and evaluated their capacity to trigger GVHD in mice.

293 d MHC-II and CD80 upregulation occurred upon GVHD induction.

294 Although currently used GVHD treatment regimens target the donor immune system,

295 As of their last follow-up visit, GVHD had resolved in all patients and no patients were r

296 zed at day 100 post-HSCT and correlated with GVHD diagnosed according to the National Institutes of H

297 BMC in nonmyeloablative conditioning without GVHD.

298 pendent, occurs in the absence of acute xeno-GVHD, highlighting the specificity of the assay, and sho

299 and provide durable prevention of xenogeneic GVHD.

300 ells are also capable of treating xenogeneic GVHD.