ライフサイエンスコーパス: GVHD

1 GVHD could be prevented by selective inactivation of Dll

2 GVHD occurred in 6 patients (30%) after nivolumab initia

3 GVHD severity was grade III-IV acute or severe chronic i

4 No patients developed acute grade 3-4 GVHD.

5 There were 7 GVHD-related deaths.

6 Acute GVHD, either grade III to IV (30 patients, 33%) or refra

7 ven patients (54%) developed grade 1-2 acute GVHD (aGVHD), none developed grade 3-4 aGVHD or chronic

8 tive incidence of skin-only, grade 1-2 acute GVHD was 30%; no patient developed extensive chronic GVH

9 ts Despite a reduction in grade 2 to 4 acute GVHD (23% v 40%; P = .004) and moderate-severe cGVHD (12

10 e cumulative incidence of grade 2 to 4 acute GVHD at day 100 was 22%, and for grade 3 to 4 it was 8%.

11 significant difference in grade 2 to 4 acute GVHD of 50% compared with a reduction in target to 28%.

12 In an acute GVHD (aGVHD) model, IL-2/mAb complexes given for only 4

13 context of alloimmune diseases such as acute GVHD has been mainly understood and managed by direct ta

14 n of overall survival when measured at acute GVHD onset (EASIX-GVHD).

15 Patients who developed acute GVHD despite maraviroc prophylaxis showed increased T-ce

16 depletion peritransplant also enhanced acute GVHD, consistent with an additional protective role for

17 were managed by standard treatment for acute GVHD.

18 pment of more effective treatments for acute GVHD.

19 signal IL-17 develop intestinal hyper-acute GVHD.

20 ss how these interactions could impact acute GVHD.

21 ed no difference between study arms in acute GVHD-free survival.

22 e incidences of severe grade III to IV acute GVHD and National Institutes of Health grade 2 to 3 chro

23 y cumulative incidence of grade III-IV acute GVHD on univariate analysis was 8%, 12%, and 17% in the

24 secondary graft failure, grade III-IV acute GVHD, non-relapse mortality by day 100, serious adverse

25 , associating with higher incidence of acute GVHD in patients undergoing AHSCT.

26 Finally, the reduction of acute GVHD lethality in mice that received Pdl1-/- donor cells

27 The mechanisms of acute GVHD regulation by the complex microbial community and t

28 that might contribute to regulation of acute GVHD severity has been largely overlooked.

29 regeneration, and mitigate severity of acute GVHD without altering the load or function of alloreacti

30 s associated with a lower incidence of acute GVHD without increased risk of disease relapse, as well

31 All 6 patients had prior history of acute GVHD.

32 f peritransplant alemtuzumab levels on acute GVHD, mixed chimerism, and lymphocyte recovery.

33 This article presents acute GVHD-related scenarios representing, respectively, certa

34 its safety and efficacy in preventing acute GVHD in settings of heightened clinical risk that use my

35 adult patients with steroid-refractory acute GVHD.

36 of MSC treatments in steroid-resistant acute GVHD.

37 ve of subsequent development of severe acute GVHD in this study.

38 he curve of 0.83) of subsequent severe acute GVHD.

39 anced the susceptibility of WT mice to acute GVHD.

40 microbiota controls susceptibility to acute GVHD.

41 In the total cohort of patients with acute GVHD (n=311), EASIX-GVHD predicted overall survival in u

42 e prediction of death in patients with acute GVHD after allogeneic stem-cell transplantation.

43 Germany and the USA) of patients with acute GVHD who had received consecutive allogeneic stem-cell t

44 future basis for development of risk-adapted GVHD treatment strategies.

45 enocytes, indicating enzyme activation after GVHD.

46 HD is a powerful predictor of survival after GVHD.

47 that maraviroc effectively protects against GVHD by modulating alloreactive donor T-cell responses,

48 sphamide (PTCy) can function as single-agent GVHD prophylaxis after myeloablative, HLA-matched relate

49 potential strategy to prevent or ameliorate GVHD.

50 ose-2,6-biphosphatase 3 (PFKFB3) ameliorated GVHD mortality and morbidity.

51 s costimulation of CD80 and PD-1 ameliorates GVHD.

52 lls and reduced interleukin 6 (P = .028) and GVHD biomarkers (Reg3, P = .041; ST2, P = .002) at day 3

53 nificantly improved rates of engraftment and GVHD following TLI/ATS/CTX compared with TLI/ATS, lethal

54 univariate analysis donor type (mother) and GVHD prophylaxis (T-cell depletion) were also significan

55 y can significantly ameliorate mucositis and GVHD.

56 emotherapy-induced intestinal mucositis, and GVHD, and speculate on possibilities of therapeutically

57 efined a nonhuman primate (NHP) large animal GVHD model.

58 Weaknesses of the animal GVHD models include the irradiation only-based condition

59 n addition to tacrolimus and methotrexate as GVHD prophylaxis.

60 d both hematopoietic target cells as well as GVHD target cells.

61 probably attributable to thrombocytopenia at GVHD onset (73 x 10(9) cells per L [IQR 29.75-180.00] fo

62 donor bone marrow was sufficient to augment GVHD caused by either TEM or TN, indicating that donor P

63 contributing to the clinical overlap between GVHD and TA-TMA.

64 one of the organs most severely affected by GVHD and research has recently highlighted the importanc

65 Importantly, the NK-cell defect induced by GVHD resulted in the failure of NK-cell-dependent in viv

66 nib effectively augments GVL without causing GVHD.

67 Compared with mice that received WT T cells, GVHD was reduced in animals that received T cells from P

68 Chronic GVHD at 1 year was zero in Tregs and 14% in controls.

69 Chronic GVHD is fundamentally caused by replacement of the host'

70 al Institutes of Health grade 2 to 3 chronic GVHD (12% and 16%, respectively) were low and associated

71 standardized the terminology around chronic GVHD classification systems to ensure that a common lang

72 Clinically, chronic GVHD is a pleiotropic, multiorgan syndrome involving tis

73 significantly exacerbates cutaneous chronic GVHD and that IL-22 is produced by highly inflammatory d

74 the composite end point of extensive chronic GVHD and relapse-free survival was significantly better

75 30%; no patient developed extensive chronic GVHD.

76 id not significantly affect risk for chronic GVHD, hematopoietic cell engraftment, overall mortality,

77 Two patients died from chronic GVHD or unrecognized drug rash with eosinophilia and sys

78 s on Criteria for Clinical Trials in Chronic GVHD standardized the terminology around chronic GVHD cl

79 ts have limited clinical efficacy in chronic GVHD, and prolonged immune suppressive treatments result

80 L-17 mediate skin GVHD, Th17-induced chronic GVHD can be attenuated by IL-22 inhibition in preclinica

81 was associated with a lower risk of chronic GVHD (26%) compared with MUD (41%; P = .04).

82 The diagnosis of chronic GVHD and determination of treatment response largely rel

83 ter transplantation, and the risk of chronic GVHD associated with HLA-matched mobilized blood cell gr

84 Cumulative incidence of chronic GVHD at 1 year was significantly lower after Haplo-HCT (

85 Treatment of chronic GVHD has previously relied primarily on corticosteroids

86 rstanding of the immune pathology of chronic GVHD offer the possibility that new therapeutic approach

87 hat HAPLO results in a lower risk of chronic GVHD than MUD transplantation.

88 e the cumulative 1-year incidence of chronic GVHD to 15% or less.

89 The cumulative incidence of chronic GVHD was 29%; relapse, nonrelapse mortality, GVHD-free r

90 The rate of a composite end point of chronic GVHD-free and relapse-free survival at 2 years was signi

91 patients, the 5-year probability of chronic GVHD-free, relapse-free survival (GRFS) is 71%.

92 ility for treatment or prevention of chronic GVHD.

93 y within 3 months after diagnosis of chronic GVHD.

94 ), none developed grade 3-4 aGVHD or chronic GVHD, and a low incidence of viral complications was obs

95 bove the median were associated with chronic GVHD compared with levels below the median in a time-dep

96 ive patients who were diagnosed with chronic GVHD.

97 d improve outcomes for patients with chronic GVHD.

98 id not result in early weight loss and colon GVHD comparable to that induced by TS1 TN, indicating th

99 9IL-33 cells) increases GVL while decreasing GVHD through two opposing mechanisms: protection from fa

100 However, patients who develop GVHD require supplemental treatment.

101 iles from human HCT recipients who developed GVHD while on immunosuppressive prophylactic agents reca

102 atient groups, but in patients who developed GVHD, T cell reactivity was skewed to target broadly exp

103 mary, PD-ligands suppress both miHA-directed GVHD and the development of alloimmunity-induced autoimm

104 ant risk of graft-versus-host (GVH) disease (GVHD).

105 A history of graft-versus-host disease (GVHD) ( n = 27) was associated with higher proportions o

106 f acute grade 2-4 graft-versus-host disease (GVHD) (21%).

107 prevent or treat graft-versus-host disease (GVHD) after allogeneic blood or marrow transplantation (

108 e risk of chronic graft-versus-host disease (GVHD) after allogeneic hematopoietic cell transplantatio

109 trol experimental graft-versus-host disease (GVHD) after allogeneic hematopoietic stem cell transplan

110 teroid-refractory graft-versus-host disease (GVHD) after allogeneic stem-cell transplantation.

111 ated to new-onset graft-versus-host disease (GVHD) after anti-PD-1.

112 ncidence of acute graft-versus-host disease (GVHD) after reduced-intensity conditioning, related dono

113 ions, principally graft-versus-host disease (GVHD) and opportunistic infections.

114 Graft-versus-host disease (GVHD) and posttransplant immunodeficiency are frequently

115 However, graft-versus-host disease (GVHD) and relapse after allo-HSCT remain major impedimen

116 delayed onset of graft-versus-host disease (GVHD) and significantly prolonged survival compared with

117 cell function and graft-versus-host disease (GVHD) are regulated via recipient invariant natural kill

118 pable of inducing graft-versus-host disease (GVHD) compared with naive T cells (TN).

119 and prevention of graft-versus-host disease (GVHD) following allogeneic hematopoietic cell transplant

120 Acute graft-versus-host disease (GVHD) grades 2-4 was more frequent when recipients or do

121 ed onset of acute graft-versus-host disease (GVHD) in a murine model, characterized by increased prol

122 rease the risk of graft-versus-host disease (GVHD) in murine models.

123 he development of graft-versus-host disease (GVHD) is a common complication of the procedure and resu

124 Graft-versus-host disease (GVHD) is a complication of allogeneic hematopoietic stem

125 Graft-versus-host disease (GVHD) is a major cause of morbidity and mortality after

126 Chronic graft versus host disease (GVHD) is a major cause of morbidity and mortality after

127 Graft-versus-host disease (GVHD) is common after allogeneic hematopoietic cell tran

128 The risk of acute graft-versus-host disease (GVHD) is higher after allogeneic hematopoietic cell tran

129 However, graft-versus-host disease (GVHD) is mediated by the same T cells and remains a sign

130 , especially when graft-versus-host disease (GVHD) is present.

131 Graft-versus-host disease (GVHD) is the major cause of nonrelapse morbidity and mor

132 stinal (GI) tract graft-versus-host disease (GVHD) is the predominant cause of morbidity and mortalit

133 However, graft-versus-host disease (GVHD) may develop when donor-derived T cells recognize a

134 ng transplant and graft-versus-host disease (GVHD) may increase risk of later malignancies of the hea

135 5-LO/LTB4 axis in graft-versus-host disease (GVHD) pathogenesis by transplanting 5-LO-deficient leuko

136 xate (Tac/Mtx) as graft-versus-host disease (GVHD) prophylaxis after matched-related allogeneic hemat

137 hamide (PT-Cy) as graft-versus-host disease (GVHD) prophylaxis has revolutionized haploidentical hema

138 Graft-versus-host disease (GVHD) prophylaxis included calcineurin inhibitor, short-

139 phosphamide-based graft-versus-host disease (GVHD) prophylaxis.

140 HSCT) and enteric graft-versus-host disease (GVHD) remain unexplored.

141 rove, but chronic graft-versus-host disease (GVHD) remains a common toxicity and major cause of nonre

142 in recent years, graft-versus-host disease (GVHD) remains a major life-threatening complication of a

143 d-resistant acute graft-versus-host disease (GVHD) remains an unmet clinical need.

144 educe the risk of graft-versus-host disease (GVHD) through reduced gastrointestinal (GI) permeability

145 foreign, causing graft-versus-host disease (GVHD) which is a main contributor to morbidity and morta

146 responses induce graft-versus-host disease (GVHD), a serious complication of allogeneic bone marrow

147 atment of chronic graft-versus-host disease (GVHD), and evidence showing the association of any propo

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

149 to rejection and graft-versus-host disease (GVHD), being overcome through transplantation of a "mega

150 avoid the risk of graft-versus-host disease (GVHD), but the genotoxicity of conditioning remains a su

151 mmunopathology in graft-versus-host disease (GVHD), however protective roles remain unclear.

152 nal mucositis and graft-versus-host disease (GVHD), these cytokines are considered pivotal during the

153 e the severity of graft-versus-host disease (GVHD), whereas costimulation of CD80 and PD-1 ameliorate

154 ses such as acute graft versus host disease (GVHD), which is the main complication of allogeneic hema

155 increased risk of graft-versus-host disease (GVHD).

156 h the often fatal graft-versus-host disease (GVHD).

157 gastrointestinal graft-versus-host disease (GVHD).

158 esulting in acute graft-versus-host disease (GVHD).

159 h a lower risk of graft-versus-host disease (GVHD).

160 ncidence of acute graft-versus-host disease (GVHD).

161 disease and acute graft-versus-host disease (GVHD).

162 ulting in harmful graft-versus-host disease (GVHD).

163 and the onset of graft-versus-host disease (GVHD).

164 aft rejection and graft-versus-host disease (GVHD); no patient received any posttransplantation GVHD

165 xed chimerism and graft-versus-host-disease (GVHD) remain limitations on success.

166 ls are active but have the capacity to drive GVHD.

167 ewer cytokine-producing donor T cells during GVHD development.

168 tion after allo-BMT was also impaired during GVHD.

169 the initiation of tissue inflammation during GVHD.

170 Thus, during GVHD, donor T cells compete with NK cells for IL-15 ther

171 t restore homeostasis in the GI tract during GVHD are highlighted.

172 During early GVHD at day+2, we found significant metabolic and cytosk

173 EASIX-GVHD could be the future basis for development of risk-a

174 educed-intensity conditioning (n=239), EASIX-GVHD was a strong predictor of overall survival (HR for

175 t of patients with acute GVHD (n=311), EASIX-GVHD predicted overall survival in univariable and multi

176 ith myeloablative conditioning (n=72), EASIX-GVHD did not predict overall survival, which is probably

177 survival and non-relapse mortality by EASIX-GVHD was successful in two independent cohorts of adult

178 s with reduced-intensity conditioning, EASIX-GVHD is a powerful predictor of survival after GVHD.

179 e validated the prognostic strength of EASIX-GVHD for overall survival and non-relapse mortality in t

180 val when measured at acute GVHD onset (EASIX-GVHD).

181 (55%) patients developed treatment-emergent GVHD after initiation of anti-PD-1 (6 acute, 4 overlap,

182 edictive of the occurrence of severe enteric GVHD (hazard ratio, 2.66; 95% confidence interval (CI) =

183 me were observed in individuals with enteric GVHD relative to those without, a finding accompanied by

184 nts with SCID and designing the approach for GVHD prophylaxis.

185 D have led to the current gold standards for GVHD prophylaxis and therapy.

186 elopment of novel therapeutic strategies for GVHD treatment.

187 Vorinostat for GVHD prevention is an effective strategy that should be

188 Full separation of GVL activity from GVHD has yet to be achieved.

189 ve approach for separating GVL activity from GVHD.

190 Risk for death from GVHD has been associated with low bacterial diversity in

191 minant cause of morbidity and mortality from GVHD after allogeneic stem cell transplantation.

192 The protection from GVHD afforded by IL-17A required secretion from, and sig

193 Moreover, protection from GVHD was attributable to augmented global reconstitution

194 GI GVHD was increased in patients with vitamin A levels bel

195 low levels of vitamin A actively promote GI GVHD and are not simply a marker of poor nutritional sta

196 ncrease in the hazard of stage 2-4 acute gut GVHD (HR, 1.22; 95% CI, 1.02-1.45; P = .03).

197 ts is associated with significantly improved GVHD colitis and survival (P < .001), conversion of MDSC

198 In GVHD target tissues, the interactions of PD-L1 with PD-1

199 Interaction of PD-L1 with PD-1 in GVHD-targeted tissues resulted in CD8+ T cell exhaustion

200 The role of interleukin (IL)-17 and IL-22 in GVHD remains uncertain, due to an apparent lack of linea

201 ly the gut microbiota, in HCT outcome and in GVHD development.

202 ant resistance mechanism to CCR5 blockade in GVHD.

203 os to enable analyses of the role of Cdk5 in GVHD, as germ line Cdk5 gene deletion is embryonically l

204 study, we have examined its contribution in GVHD pathogenesis.

205 ed suppressor cells (MDSCs) were enriched in GVHD target organs.

206 ndogenous thymic regeneration is impaired in GVHD.

207 We found that the thymopoietic impairment in GVHD associated with loss of ILCs could be improved by r

208 2 after allogeneic transplantation mainly in GVHD typical target organs skin, liver, and intestines,

209 or bone marrow-derived CD70 plays no role in GVHD, host-derived CD70 inhibits GVHD as CD70(-/-) hosts

210 reased treatment-related mortality including GVHD, infections, and organ failure after allo-HCT.

211 ical HSCT without adverse effects, increased GVHD, or higher mortality, and was associated with signi

212 CD70(-/-) hosts show significantly increased GVHD.

213 er, these results suggest that the increased GVHD risk after unrelated HCT is predominantly an effect

214 CD70 after allo-HCT significantly increases GVHD.

215 el minor histocompatibility Ag (miHA) induce GVHD in miHA-positive recipients, we found that cell-int

216 The patients with nivolumab-induced GVHD were managed by standard treatment for acute GVHD.

217 no role in GVHD, host-derived CD70 inhibits GVHD as CD70(-/-) hosts show significantly increased GVH

218 20% increase in the hazard of grades III-IV GVHD (hazard ratio [HR], 1.20; 95% confidence interval [

219 to test the hypothesis that TEM induce less GVHD because of increased sensitivity to PD-ligands.

220 In a BALB/c --> B6 lethal GVHD model, adoptive transfer of MDSCs from TLI/ATS/CTX-

221 d TS1 TEM induced more severe skin and liver GVHD in the absence of PD-ligands.

222 l strategies to enhance GVL while minimizing GVHD following allogeneic HCT.

223 GVHD was 29%; relapse, nonrelapse mortality, GVHD-free relapse-free survival, and overall survival at

224 effects in allogeneic and xenogeneic murine GVHD models.

225 Using an established, preclinical, murine, GVHD model, we reveal that Cdk5 activity is increased in

226 or immune cell population in the context of GVHD.

227 ntal approaches, we observed that control of GVHD by Tregs was fully abolished by blocking TNF recept

228 Here, we show that the development of GVHD after allo-BMT prevented NK-cell reconstitution, pa

229 n whether TME plays a role in development of GVHD after HSCT.

230 ution of Cdk5 activity to the development of GVHD has not been explored.

231 ective GVL reactivity without development of GVHD.

232 sient chimerism-based tolerance is devoid of GVHD risk and appears to initially depend on regulatory

233 ioning therapy, resulting in exacerbation of GVHD.

234 lenocytes resulted in increased incidence of GVHD in RIC mice.

235 g a significant increase in the incidence of GVHD, we studied donor-derived CD19 CAR T cells in allo-

236 loantigen-activated T cells and induction of GVHD, as inhibition of glycolysis by targeting mTORC1 or

237 eviously, in the TS1 TCR transgenic model of GVHD, wherein TS1 CD4 cells specific for a model minor h

238 -HCT, findings generated in animal models of GVHD have led to the current gold standards for GVHD pro

239 and colleagues used several murine models of GVHD to evaluate the effect of CD4+ T cell depletion on

240 at it may increase risk of the occurrence of GVHD, although this has not been reported in selected pa

241 n, and significantly decreased occurrence of GVHD.

242 ated CAR T cells increased the occurrence of GVHD.

243 trate that the BM is a major target organ of GVHD in an informative clinically relevant RIC mouse maj

244 nces in understanding the pathophysiology of GVHD.

245 Conversion of chimerism in the presence of GVHD after CD4 donor lymphocyte infusion was observed in

246 vity after DLI in the absence or presence of GVHD.

247 ligands has emerged as a major regulator of GVHD pathogenesis, little is known about the timing of e

248 Two patients died as a result of GVHD, 1 of progressive disease and 1 of complications re

249 e findings could explain the reduced risk of GVHD occurring with cumulative TCR and CAR signaling.

250 H mismatching correlate with higher risks of GVHD after allogeneic HCT.

251 The estimated risks of GVHD-related outcomes in HLA-phenotypically matched unre

252 In contrast, the risks of GVHD-related outcomes were higher in HLA-DP GVH-mismatch

253 t could be informative as to the severity of GVHD and its response to therapy.

254 hibitors are ineffective in the treatment of GVHD after LT.

255 Prevention and treatment of GVHD remain inadequate and commonly lead to end-organ dy

256 ic strategies as prophylaxis or treatment of GVHD.

257 ences were associated with a history of oral GVHD and a history of oral mucositis.

258 vidence that the 5-LO/LTB4 axis orchestrates GVHD development and suggest it could be a target for th

259 ed the severity of systemic and target organ GVHD.

260 ee conditions, and the lack of pharmacologic GVHD prevention in control groups.

261 no patient received any posttransplantation GVHD prophylaxis.

262 n TME is associated with posttransplantation GVHD in patients with SCID.

263 exhaustion and apoptosis, thereby preventing GVHD, whereas PD-L1 interactions with CD80 in lymphoid t

264 xhaustion, and apoptosis, thereby preventing GVHD.

265 ic cell transplantation effectively prevents GVHD while preserving strong graft-versus-leukemia (GVL)

266 Patients received GVHD prophylaxis with tacrolimus and methotrexate.

267 g in murine HSCT models dramatically reduced GVHD and improved graft survival.

268 on treatment had prolonged survival, reduced GVHD clinical scores, reduced intestinal and liver injur

269 Refractory GVHD affects survival but not within the confined ICU ad

270 pid onset of severe and treatment-refractory GVHD.

271 ble admission criteria, especially regarding GVHD.

272 D-ligand-expressing APCs critically regulate GVHD.

273 sion for patients predicted to have low-risk GVHD are safe and effective.

274 Sclerotic GVHD has clinical and histopathological similarities wit

275 ated with conversion of chimerism and severe GVHD.

276 oreactive TEM TS1 TN also caused more severe GVHD without PD-ligands.

277 -derived IL-22 in patients with chronic skin GVHD and confirm parallel but symbiotic developmental pa

278 tly, while both IL-22 and IL-17 mediate skin GVHD, Th17-induced chronic GVHD can be attenuated by IL-

279 ntemporary control cohort receiving standard GVHD prophylaxis alone.

280 of reduced-intensity allo-HSCT with standard GVHD prophylaxis plus maraviroc to a contemporary contro

281 As in prior studies, GVHD was associated with lower alpha diversity of the st

282 ol was positively correlated with subsequent GVHD; Lachnospiraceae were negatively correlated.

283 emonstrate in experimental mouse models that GVHD results in depletion of intrathymic group 3 innate

284 ntrinsic properties of TS1 TEM reduced their GVHD potency relative to TS1 TN Posttransplant, TS1 TEM

285 se 17 patients achieved complete response to GVHD treatment, and 14 of 17 required >/=2 systemic ther

286 insights into the biology of lower GI tract GVHD and focus on intrinsic pathways and regulatory mech

287 Recent data indicate that lower GI tract GVHD is a complicated process mediated by donor/host ant

288 picobirnaviruses with early post-transplant GVHD.

289 d correlated with higher fecal levels of two GVHD severity markers, calprotectin and alpha1-antitryps

290 prospective, multicenter study with uniform GVHD prophylaxis, conditioning regimen, and donor source

291 ffect of CD4+ T cell depletion on GVL versus GVHD and revealed that depletion of CD4+ T cells leads t

292 viroc results in a low incidence of visceral GVHD.

293 to assist clinicians in managing adults with GVHD after LT.

294 ing the course of HCT and is associated with GVHD development and treatment with broad-spectrum antib

295 owever, the specific species associated with GVHD risk remain poorly defined.

296 in the intestinal flora are associated with GVHD, bacteremia, and reduced overall survival after all

297 pared with syngeneic controls, RIC mice with GVHD showed evidence of BM suppression, have anemia, red

298 ion are present in the skin of patients with GVHD after allo-SCT.

299 tients with selective GVL reactivity without GVHD.

300 compared with transplant recipients without GVHD, thereby inhibiting IL-22-mediated protection of th