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1 showed similar incidences of grades II to IV acute graft-versus host disease.
2 dex (EASIX) was shown to predict death after acute graft-versus-host disease.
3 cell source and donor type, age and grade of acute graft-versus-host disease.
4 53 patients (17%) developed grades II to IV acute graft-versus-host disease.
5 ently in the treatment of steroid-refractory acute graft-versus-host disease.
6 a systemic bacterial infection, colitis, and acute graft-versus-host disease.
7 f the five children had grade II, III, or IV acute graft-versus-host disease.
8 patibility complex barriers without inducing acute graft-versus-host disease.
9 monia syndrome-like phenotype and aggravated acute graft-versus-host disease.
10 associated with a higher risk of developing acute graft-versus-host disease.
11 nd death (P = 0.002), but a similar risk for acute graft-versus-host disease.
16 (AT) was capable of protecting animals from acute graft-versus-host disease (aGVHD) across major his
18 R-181a expression in donor T cells may alter acute graft-versus-host disease (aGvHD) after allogeneic
20 pients were followed for disease relapse and acute graft-versus-host disease (aGvHD) development post
21 e lower incidence and severity of high-grade acute graft-versus-host disease (aGVHD) exhibited by UCB
22 arly diagnosis, prevention, and treatment of acute graft-versus-host disease (aGVHD) have been transl
24 T cells have improved survival and decreased acute graft-versus-host disease (aGVHD) in 2 different m
26 eg cells protects recipient mice from lethal acute graft-versus-host disease (aGVHD) induced by donor
27 ective therapy for hematologic malignancies, acute graft-versus-host disease (aGVHD) is a leading cau
28 Steroid refractory gastrointestinal (GI) acute graft-versus-host disease (aGVHD) is a major cause
40 ty and mortality from clinically significant acute graft-versus-host disease (aGVHD) remains a limita
43 elopment of severe and/or steroid-refractory acute graft-versus-host disease (aGVHD) remains a signif
44 helial adhesion molecule induction in murine acute graft-versus-host disease (aGVHD) revealed unexpec
45 ly reported that dermal papillary vessels in acute graft-versus-host disease (aGVHD) support shear-re
47 OS), cumulative incidence of engraftment and acute graft-versus-host disease (aGVHD) within the first
48 geneic hematopoietic cell transplantation is acute graft-versus-host disease (aGVHD), a devastating c
49 lantation viral reactivation, grade II to IV acute graft-versus-host disease (aGvHD), and chronic gra
51 conditioning (with vs. without irradiation), acute graft-versus-host disease (aGVHD), or chronic graf
64 5% CI, 1.50-5.55; P = 0.002) and grade II-IV acute graft-versus-host disease (aHR, 1.59; 95% CI, 1.06
65 ster myeloid and platelet recovery and lower acute graft versus host disease and may reduce the total
66 fied according to the presence or absence of acute graft-versus-host disease and CMV DNA in plasma.
67 suggest a novel mechanism explaining reduced acute graft-versus-host disease and improvement in autoi
68 nuated clinical symptoms in animal models of acute graft-versus-host disease and multiple sclerosis.
69 er transplant-related complications, such as acute graft-versus-host disease and opportunistic infect
70 or CMV reactivation, including patients with acute graft-versus-host disease and those receiving ster
72 l transplantation without steroid-refractory acute graft-versus-host disease and without early relaps
73 , whereas infection, veno-occlusive disease, acute graft-versus-host disease, and death were predicte
75 cumulative incidence of grade II, III, or IV acute graft-versus-host disease at 100 days was 64 perce
77 spital stay; intensive care unit admissions; acute graft-versus-host disease; Bearman toxicity score;
78 ith a naive phenotype in patients developing acute graft-versus-host disease, compared with tolerant
79 om a skin biopsy of a patient suffering from acute graft-versus-host disease following sex-mismatched
80 nig and colleagues1 demonstrate in mice that acute graft-versus-host disease (GHVD) results in a mark
81 ity (cytopenias) was reported in 4 patients, acute graft-versus-host disease grade 1 in 2, grade 2 in
87 ich they influence disease processes such as acute graft versus host disease (GVHD), which is the mai
90 sis was greater in patients with grade II-IV acute graft-versus-host disease (GVHD) (33.9% +/- 11.3%)
91 V (60% vs 24%, P = .01) and grades III to IV acute graft-versus-host disease (GVHD) (47% vs 14%, P =
92 ce of neutrophil recovery at day 60 was 91%, acute graft-versus-host disease (GVHD) (grade II-IV) at
95 lls (DC) are important in the development of acute graft-versus-host disease (GVHD) after allogeneic
96 10RB) gene with development of grades III-IV acute graft-versus-host disease (GVHD) after allogeneic
97 (BMT) recipients are at heightened risk for acute graft-versus-host disease (GVHD) after allogeneic
98 ompatibility antigen HA-1 is associated with acute graft-versus-host disease (GVHD) after allogeneic
99 us antithymocyte serum protects mice against acute graft-versus-host disease (GVHD) after hematopoiet
100 rriage correlates with increased severity of acute graft-versus-host disease (GVHD) after matched unr
101 tat) is safe and results in low incidence of acute graft-versus-host disease (GVHD) after reduced-int
103 o percent of patients developed grade 2 to 4 acute graft-versus-host disease (GVHD) and 74% extensive
104 the recipient is associated with less severe acute graft-versus-host disease (GVHD) and a lower risk
105 f T-bet and IFN-gamma in T cell responses in acute graft-versus-host disease (GVHD) and found that T-
106 factor, was tested for potential benefits on acute graft-versus-host disease (GVHD) and hematopoietic
107 There exists a strong association between acute graft-versus-host disease (GVHD) and IPS, and bron
111 0, SCD) had slower neutrophil recovery, less acute graft-versus-host disease (GVHD) and none had exte
112 The 6-month probabilities of grade 3 or 4 acute graft-versus-host disease (GVHD) and nonrelapse mo
113 prognostic information about development of acute graft-versus-host disease (GVHD) and subsequent mo
114 , Cav-1(-/-)donor T cells caused less severe acute graft-versus-host disease (GVHD) and yielded highe
116 ates, kinetics of engraftment, toxicity, and acute graft-versus-host disease (GVHD) associated with a
119 The cumulative incidence of grade 2 to 4 acute graft-versus-host disease (GVHD) at day 100 was 44
122 e alloantigen-driven parent-into F1 model of acute graft-versus-host disease (GVHD) characterized by
123 t 4-fold lower in patients with grade 2 to 4 acute graft-versus-host disease (GVHD) compared with pat
130 er induction chemotherapy and the absence of acute graft-versus-host disease (GVHD) development follo
131 10-fold higher dose of transplanted T cells, acute graft-versus-host disease (GVHD) does not develop
132 Five of 9 transplant recipients experienced acute graft-versus-host disease (GVHD) following aNK-DLI
142 nal role of Th17 cells in the development of acute graft-versus-host disease (GVHD) has not been well
143 as second-line therapy for the treatment of acute graft-versus-host disease (GVHD) in 21 patients (1
144 ood, Shah et al describe the onset of severe acute graft-versus-host disease (GVHD) in 5 of 9 patient
145 e (GF) occurred in 26 patients (16%), severe acute graft-versus-host disease (GVHD) in 9 (6%), and ch
146 nterleukin-18 (IL-18) regulates experimental acute graft-versus-host disease (GVHD) in a Fas-dependen
147 bone marrow transplantation (BMT) attenuates acute graft-versus-host disease (GVHD) in a lethally irr
148 O T cells also mediated accelerated onset of acute graft-versus-host disease (GVHD) in a murine model
150 ory T cells (Tregs) has been used to prevent acute graft-versus-host disease (GVHD) in mice and has s
151 in vitro and whether those cells can inhibit acute graft-versus-host disease (GVHD) in vivo upon adop
166 revious experimental studies have shown that acute graft-versus-host disease (GVHD) is associated wit
168 SP) and methotrexate (MTX), the incidence of acute graft-versus-host disease (GVHD) is greater than 7
172 an important secondary lymphoid organ where acute graft-versus-host disease (GVHD) is initiated by d
173 complication of solid organ transplantation, acute graft-versus-host disease (GVHD) is most associate
174 reased numbers of T cells in the PBSC graft, acute graft-versus-host disease (GVHD) is not increased.
190 marker-based tools may identify a lower-risk acute graft-versus-host disease (GVHD) population amenab
191 g trial, 27 patients with steroid-refractory acute graft-versus-host disease (GVHD) received ABX-CBL
193 sttransplantation immunosuppressive therapy, acute graft-versus-host disease (GVHD) remains a major c
201 on, specifically whether prophylaxis through acute graft-versus-host disease (GVHD) results in improv
203 ciating graft-versus-tumor (GVT) effect from acute graft-versus-host disease (GVHD) still remains a g
204 nal signature of T cells during breakthrough acute graft-versus-host disease (GVHD) that occurs in th
206 omarkers are associated with the response of acute graft-versus-host disease (GVHD) to therapy after
210 Further, the incidence of grades III to IV acute graft-versus-host disease (GVHD) was significantly
211 cumulative incidences of grades 2, 3, and 4 acute graft-versus-host disease (GVHD) were 38%, 9%, and
212 , 17 patients with glucocorticoid-refractory acute graft-versus-host disease (GVHD) were enrolled in
213 ere confirmed in vivo using a mouse model of acute graft-versus-host disease (GVHD) wherein host DCs
214 We hypothesized that initial treatment of acute graft-versus-host disease (GVHD) with low-dose glu
215 ation (BMT) resulted in marked inhibition of acute graft-versus-host disease (GVHD) with retention of
216 topoietic cell transplantation is limited by acute graft-versus-host disease (GvHD), a severe complic
217 nces of neutrophil engraftment, grades II-IV acute graft-versus-host disease (GVHD), and chronic GVHD
218 ll IFN-gamma production correlated with more acute graft-versus-host disease (GVHD), and decreased KI
219 he major cause of morbidity and mortality in acute graft-versus-host disease (GVHD), and pathological
220 teroids are the accepted primary therapy for acute graft-versus-host disease (GVHD), but durable resp
221 , with primary risk factors including severe acute graft-versus-host disease (GVHD), chronic extensiv
222 f HLA-A, B, or C, on the risks for grade 3-4 acute graft-versus-host disease (GVHD), chronic GVHD, tr
223 in improving engraftment without increasing acute graft-versus-host disease (GVHD), despite much lar
225 ortant causes of diarrhea after HSCT include acute graft-versus-host disease (GVHD), infections, and
227 There was no impact of EBV reactivation on acute graft-versus-host disease (GVHD), nonrelapse morta
228 ointestinal tract are major target organs of acute graft-versus-host disease (GVHD), the major compli
229 KIR-L mismatch had no effect on grade III-IV acute graft-versus-host disease (GVHD), transplantation-
230 responses of allogeneic BM donors may affect acute graft-versus-host disease (GVHD), we investigated
231 ients developed grade C (n = 4) or D (n = 1) acute graft-versus-host disease (GVHD), with only one at
249 HSCT, broad-spectrum antimicrobial use, and acute graft-versus-host disease (GVHD; adjusted odds rat
250 Thirty-eight percent of patients developed acute graft-versus-host disease (GVHD; grade II in all b
251 IR3DS1 was associated with lower-grade II-IV acute graft-versus-host disease (GVHD; odds ratio = 0.71
252 icted a greater risk of developing grade 3-4 acute graft-versus-host disease (GVHD; RR = 1.58, 95% CI
254 In hematopoietic stem cell transplantation, acute graft-versus-host-disease (GVHD) is caused by an a
255 alyzed with respect to tempo of engraftment, acute graft-versus-host-disease (GVHD), clinical extensi
257 y; acute toxicity (veno-occlusive disease or acute graft versus-host disease [GvHD]); chronic GvHD; o
258 G was associated with decreased incidence of acute graft-versus-host disease (hazard ratio [HR], 0.31
259 associated with an increased risk of severe acute graft-versus-host disease (HR = 1.43, P = 0.730).
260 d mortality (HR = 1.54, 1.54), and grade 3-4 acute graft-versus-host disease (HR = 1.49, 1.77) compar
264 and Treg cells in association with clinical acute graft-versus-host disease in allogeneic hematopoie
265 fectively suppress inflammatory responses in acute graft-versus-host disease in humans and in a numbe
266 mAb against PD-1H, which strikingly prevents acute graft-versus-host disease in semi- and fully allog
267 idence interval, 1.84-31.7), controlling for acute graft-versus-host disease, in 109 patients with Ph
268 h in vitro and in vivo, including inhibiting acute graft-versus-host disease induced by allogeneic CD
269 he role of IL-18 in three disease processes (acute graft-versus-host disease, insulin-dependent diabe
272 c graft-versus-host disease (cGVHD) and late acute graft-versus-host disease (L-aGVHD) are understudi
275 Five patients had grade II or grade III acute graft-versus-host disease; none had extensive chro
276 required no platelet or RBC transfusion, and acute graft-versus-host disease of greater than grade 2
277 ppeared to be independent of CMV viral load, acute graft-versus-host disease, or ganciclovir-associat
278 , reduced-intensity conditioning (P = 0.02), acute graft-versus-host disease (P = 0.03), and chronic
280 aper, we show human CD4/CD8 double-positive, acute graft-versus-host disease-protective, minor H Ag-s
282 survival or in the incidence or severity of acute graft-versus-host disease regardless of exposure t
288 rominent among patients who developed severe acute graft-versus-host disease, suggesting that short t
290 the armamentarium against steroid-refractory acute graft-versus-host disease, the prognosis of this e
295 serum level of cyclosporine, infections, and acute graft versus host disease were compared statistica
297 mia or myelodys-plastic syndrome, and severe acute graft-versus-host disease were associated with sig
298 er risks of LONIPC, but age, graft type, and acute graft-versus-host disease were not identified as r
299 lymphocyte count <300 cells/uL at D +30, and acute graft-versus-host disease were predictors of ADV v