ライフサイエンスコーパス: graft-vs-host disease

1 arrow, and there was no evidence of clinical graft vs host disease.

2 rm tolerance or developed late-onset chronic graft-vs-host disease.

3 adiation toxicity, but also protects against graft-vs-host disease.

4 sponses, such as platelet refractoriness and graft-vs-host disease.

5 e chimerism without causing acute or chronic graft-vs-host disease.

6 emely limited repertoire of Ags can initiate graft-vs-host disease.

7 from kidneys of animals with murine chronic graft-vs-host disease.

8 similar to lesions associated with cutaneous graft-vs-host disease.

9 e donor engraftment without acute or chronic graft-vs-host disease.

10 with continued stable donor chimerism and no graft-vs-host disease.

11 in the treatment of allograft rejection and graft-vs-host disease.

12 unity of both donor and host T cells without graft-vs-host disease.

13 t disease, demonstrating that LC can trigger graft-vs-host disease.

14 of pathological changes in a human model of graft-vs-host disease.

15 tions and tumors as well as autoimmunity and graft-vs-host disease.

16 of T cell-mediated autoimmune disorders and graft-vs-host disease.

17 on tolerance across MHC disparities, without graft-vs-host disease.

18 mune disease that at times resembles chronic graft-vs-host disease.

19 ic BMT by contributing to the development of graft vs. host disease.

20 in autoimmune diseases, transplantation, and graft vs. host disease.

21 nsplantation, but can cause life-threatening graft-vs.-host disease.

22 In a mouse model of graft-vs-host disease, 16.4 +/- 2.7% of CD8 cells that i

23 drome (22 eyes), Sjogren syndrome (11 eyes), graft-vs-host disease (2 eyes), dry eye after keratomile

24 immunity and enhance GvL without increasing graft-vs-host disease activity.

25 When chronic graft-vs-host disease affects the lung tissue, bronchiol

26 the PBL of a patient suffering from chronic graft-vs-host disease after bone marrow transplant from

27 gen-primed effector memory T cells to induce graft-vs-host disease after bone marrow transplantation

28 tural suppressor" T cells protect hosts from graft-vs-host disease after the infusion of allogeneic b

29 ne studies have found acute gastrointestinal graft-vs-host disease (aG-GVHD) to be associated with in

30 l of CTL development, parent-into-F(1) acute graft-vs-host disease (AGVHD), to evaluate this issue.

31 By quantifying graft-vs-host disease alloresponses in vivo, we demonstr

32 ne alone, were markedly impaired in inducing graft-vs-host disease alloresponses to MHC class II disp

33 nd thereby cause chronic graft rejection and graft-vs-host disease among MHC identical individuals.

34 could serve as an ideal strategy to prevent graft-vs-host disease and allograft rejection or to trea

35 tocompatibility (H) Ag disparities result in graft-vs-host disease and chronic solid allograft reject

36 uman allogeneic bone marrow transplantation, graft-vs-host disease and graft rejection can occur even

37 BB represents a new approach to altering the graft-vs-host disease and graft-vs-leukemia effects of a

38 erapeutic for organ transplant recipients or graft-vs-host disease and is an approved therapeutic for

39 ll (DC) functions and regulates experimental graft-vs-host disease and other immune-mediated diseases

40 l populations have the potential to suppress graft-vs-host disease and stimulate antitumor responses.

41 treated T cells lost their ability to induce graft-vs-host disease and, instead, prevented other pare

42 ly in primate models of allograft rejection, graft-vs-host disease, and autoimmunity.

43 erred into semiallogeneic mice fail to cause graft-vs-host disease, and when injected into syngeneic,

44 te chimerism; incidence of acute and chronic graft-vs-host disease; and sickle cell-thalassemia disea

45 ls in cyclosporin A (CSA)-induced autologous graft-vs-host disease are recent thymic emigrants (RTEs)

46 , neutrophil recovery, and acute and chronic graft-vs-host disease, as ascertained by transplant cent

47 8%; HR, 0.77; 95% CI, 0.48-1.23), or chronic graft-vs-host disease at 1-year (cumulative incidence, 2

48 Cyclosporin A (CSA)-induced autologous graft-vs-host disease (autoGVHD) is an autoimmune syndro

49 lone is characterized by a decreased risk of graft-vs-host disease but increased incidence of engraft

50 rventions to control autoimmune diseases and graft vs. host disease, but oversuppression of these pat

51 ortant role in pathogenesis of human chronic graft vs. host disease (cGVHD).

52 parent-into-F(1) (p-->F(1)) model of chronic graft-vs-host disease (cGVHD) in which lupus-like humora

53 Chronic graft-vs-host disease (cGVHD) is an increasingly frequen

54 Chronic graft-vs-host-disease (cGVHD) after allogeneic stem cell

55 Importance: Chronic graft-vs-host-disease (cGVHD) after allogeneic stem cell

56 Chronic graft-vs.-host disease (cGVHD) is a complication of allo

57 nocytes had 40% early mortality due to acute graft-vs-host disease compared with no deaths among reci

58 ve pretreatment regimens, graft failure, and graft-vs-host disease complicate the utility of BMT for

59 replaced by donor cells, exhibit marked skin graft-vs-host disease, demonstrating that LC can trigger

60 vs 85%; HR, 0.94; 95% CI, 0.73-1.22), acute graft-vs-host disease grades III-IV at 100 days (cumulat

61 been detected in mice, the ability to induce graft vs host disease (GVHD) after bone marrow transplan

62 risk for grades II to IV and III to IV acute graft vs host disease (GVHD), chronic GVHD, transplant-r

63 ansplant, T-cell depletion and variations in graft vs. host disease (GVHD) prophylaxis.

64 Chronic graft-vs-host disease (GVHD) affects 50% to 70% of patie

65 t-vs-leukemia (GVL) response but also induce graft-vs-host disease (GVHD) after allogeneic bone marro

66 Graft-vs-host disease (GVHD) after allogeneic bone marro

67 approach being evaluated for the control of graft-vs-host disease (GVHD) after allogeneic bone marro

68 at could be important for the development of graft-vs-host disease (GVHD) after bone marrow transplan

69 ner as naive T cells with respect to causing graft-vs-host disease (GVHD) and facilitating engraftmen

70 Rapamycin (sirolimus) inhibits graft-vs-host disease (GVHD) and polarizes T cells towar

71 NF/TNFR2 interactions ameliorates intestinal graft-vs-host disease (GVHD) and Th1 cytokine responses

72 Cutaneous manifestations of chronic graft-vs-host disease (GvHD) are highly variable and may

73 F(1)) model of acute or chronic (lupus-like) graft-vs-host disease (GVHD) as a model of either a CTL-

74 Lethal graft-vs-host disease (GVHD) can be induced between MHC-

75 been used to elucidate the immunobiology of graft-vs-host disease (GVHD) following allogeneic bone m

76 ponses, the role of CD30/CD153 in regulating graft-vs-host disease (GVHD) has not been reported.

77 regs), shown functionally as exacerbation of graft-vs-host disease (GVHD) in mice.

78 -vs-leukemia (GVL) activity, but also induce graft-vs-host disease (GVHD) in recipients conditioned w

79 To study the character of graft-vs-host disease (GVHD) induced by T cells specific

80 he parent-into-immunocompetent-F(1) model of graft-vs-host disease (GVHD) induces immune dysregulatio

81 Graft-vs-host disease (GVHD) is a major complication of

82 Graft-vs-host disease (GVHD) is a pathological process i

83 Graft-vs-host disease (GVHD) is caused by a donor T cell

84 Graft-vs-host disease (GVHD) is caused by activated dono

85 Graft-vs-host disease (GVHD) is caused by activated dono

86 Similarly, graft-vs-host disease (GVHD) is distinct in inbred murin

87 ry tests for the diagnosis and monitoring of graft-vs-host disease (GVHD) is hampered by a lack of kn

88 Acute graft-vs-host disease (GVHD) is influenced by pathways t

89 ar and molecular determinants that influence graft-vs-host disease (GVHD) is not known.

90 Graft-vs-host disease (GVHD) is the leading cause of tre

91 Graft-vs-host disease (GVHD) is the major cause of morbi

92 Here we studied the role of ICOS in graft-vs-host disease (GVHD) mediated by CD4(+) or CD8(+

93 In vivo studies using a murine graft-vs-host disease (GVHD) model demonstrated that WN

94 ponses, is under investigation in humans for graft-vs-host disease (GVHD) prevention.

95 h between several mechanisms responsible for graft-vs-host disease (GVHD) protection in anti-CD3epsil

96 ive treatment for leukemia and lymphoma, but graft-vs-host disease (GVHD) remains a major complicatio

97 Graft-vs-host disease (GVHD) remains the most life-threa

98 r T cells, but whether IL-7 also exacerbates graft-vs-host disease (GVHD) remains unresolved.

99 nce was also demonstrated to be operative in graft-vs-host disease (GVHD) responses against BALB.B-de

100 Acute graft-vs-host disease (GVHD) results from the activation

101 MT can mediate a potent GVL effect with less graft-vs-host disease (GVHD) than would be observed if g

102 Acute graft-vs-host disease (GVHD) typically requires high-dos

103 anti-TNF-alpha mAb to mice undergoing acute graft-vs-host disease (GVHD) using the parent-into-F(1)

104 rs for allogeneic transplant recipients, and graft-vs-host disease (GVHD) was assessed.

105 he parent-into-F1 model of acute and chronic graft-vs-host disease (GVHD) was used as an example of i

106 ents, allogeneic HCT recipients with chronic graft-vs-host disease (GvHD) were at increased risk of f

107 ics, risk factors for, and impact of chronic graft-vs-host disease (GVHD) were evaluated in a consecu

108 hed donor bone marrow (BM) graft exacerbated graft-vs-host disease (GVHD) when DLI was administered a

109 dels, this ex vivo sFasL treatment abrogated graft-vs-host disease (GVHD) while sparing donor T cells

110 implicated in the pathophysiology of chronic graft-vs-host disease (GVHD), and phase 2 trials suggest

111 immunotoxins (ITs) in the therapy of cancer, graft-vs-host disease (GvHD), autoimmune diseases, and A

112 tissue damage during allograft rejection and graft-vs-host disease (GVHD), but its role in supporting

113 quired for initiating T cell-dependent acute graft-vs-host disease (GVHD), but the role of APCs in th

114 has a major role in the development of acute graft-vs-host disease (GVHD), Fas ligand-deficient (gld)

115 the parent-into-F1 model of acute or chronic graft-vs-host disease (GVHD), respectively.

116 parent-into-F(1) (P-->F(1)) model of chronic graft-vs-host disease (GVHD), using wild-type or TRAIL-d

117 , and ICOS regulate the development of acute graft-vs-host disease (GVHD), we wished to assess if BTL

118 Tg mice developed autoreactive skin disease (graft-vs-host disease (GVHD)-like skin lesions) while K1

119 es during preconditioning and development of graft-vs-host disease (GVHD).

120 transplants (BMT) without significant acute graft-vs-host disease (GvHD).

121 ivated CD8 lymphocytes is a major feature of graft-vs-host disease (GvHD).

122 c progenitor cell transplants, but may cause graft-vs-host disease (GVHD).

123 in combination to mice with parent-into-F(1) graft-vs-host disease (GVHD).

124 have been shown to undergo apoptosis during graft-vs-host disease (GVHD).

125 s recognizing host alloantigen and mediating graft-vs-host disease (GVHD).

126 , DLIs are associated with a reduced risk of graft-vs-host disease (GVHD).

127 ts a systemic autoimmune syndrome resembling graft-vs-host disease (GVHD).

128 te both a graft-vs-leukemia (GVL) effect and graft-vs-host disease (GVHD).

129 emia (GVL) effects but often leads to severe graft-vs-host disease (GVHD).

130 sponses by dendritic cells (DCs) and prevent graft-vs-host disease (GVHD).

131 n attack nonmalignant host tissues and cause graft-vs-host disease (GVHD).

132 mbers of IFN-gamma(+) cells without inducing graft-vs-host disease (GVHD).

133 into B6D2F1 mice induces chronic lupus-like graft-vs-host disease (GVHD).

134 requently associated with the development of graft-vs-host disease (GVHD).

135 crease the risk of relapse without enhancing graft-vs-host disease (GVHD).

136 es mortality in MHC class I and II disparate graft-vs-host disease (GVHD).

137 ted migration of alloreactive T cells during graft-vs-host disease (GVHD).

138 ession on host APCs is essential to initiate graft-vs-host disease (GVHD); however, critical APC subs

139 tment (median, 68.3%) associated with severe graft-vs-host disease (GvHD; 62 vs 0% with TCDBM alone).

140 iciency disorders, yet complications such as graft-vs.-host disease (GvHD) limit survival.

141 hown to achieve anti-tumor responses without graft-vs.-host disease (GVHD).

142 uding control of infections without inducing graft-vs.-host disease (GVHD).

143 geneic bone marrow transplant (BMT) -induced graft-vs.-host disease (GvHD).

144 tacking healthy host tissues, termed chronic graft-vs-host disease, has become a more common phenomen

145 , 35.08 [95% CI, 3.90-315.27]), grade III/IV graft-vs-host disease (HR, 16.50 [95% CI, 2.67-102.28]),

146 responsible for chronic graft rejection and graft vs host disease in solid tissue and bone marrow tr

147 activity of donor T cells without increased graft-vs-host disease in both MHC- and minor histocompat

148 regs that consistently suppressed xenogeneic graft-vs-host disease in immunodeficient mice.

149 sion by human Tregs in a model of xenogeneic graft-vs.-host disease induced by the transfer of human

150 a recipient alloantigen, thereby preventing graft-vs-host disease initiated by a TCR-transgenic T ce

151 ate that tolerance to CSA-induced autologous graft-vs-host disease is actively mediated by CD25+CD4+

152 the nephritogenic T cell response in chronic graft-vs-host disease is autoreactive in nature and may

153 the fate of alloreactive T cell effectors in graft-vs-host disease, Ld-specific CD8+ T cells from C57

154 uncommon, consisting of oral lichen planus, graft-vs-host disease-like colitis, and pure red cell ap

155 ly autoreactive T cells and development of a graft-vs-host-disease-like syndrome.

156 l allograft rejection and maternal antifetal graft-vs-host disease mechanisms.

157 A chronic graft-vs-host disease model also showed that Sle1c produ

158 he same two loci identified with the chronic graft-vs-host disease model, excluding the Cr2 region.

159 ators as well as proliferation in an in vivo graft-vs-host disease model.

160 cells into effector cells in an experimental graft-vs.-host disease mouse model.

161 ds ratio, 11.3; P < .01), acute (grade >/=2) graft-vs-host disease (odds ratio, 8.2; P < .02) and mis

162 (MPO) in tear washes of patients with ocular graft-vs-host disease (oGVHD).

163 ssociated with increases in acute or chronic graft-vs-host disease or organ toxicities.

164 Patients with chronic graft-vs-host disease (P =.01), with less social support

165 ations include vascular barrier dysfunction, graft-vs-host disease, platelet activation, ischemia, an

166 eas older age, extranodal disease, and acute graft-vs-host disease predicted poor outcome.

167 Factors such as primary disease, chronic graft-vs-host disease, prolonged immunosuppression, radi

168 which may account, in part, for the partial graft-vs-host disease protective effect of anti-CD40L mA

169 e regimen intensity, but graft rejection and graft-vs-host disease remain significant.

170 iverse as erythema nodosum leprosum, chronic graft-vs-host disease, rheumatoid arthritis, and sarcoid

171 oughly characterize a murine sclerodermatous graft-vs-host disease (Scl GVHD) model for scleroderma t

172 Murine sclerodermatous graft-vs-host disease (Scl GVHD) models human scleroderm

173 Syngeneic graft-vs-host disease (SGVHD) develops following lethal

174 Syngeneic graft-vs-host disease (SGVHD) is induced by reconstituti

175 ntory, occupational functioning, Lee Chronic Graft-vs-Host Disease Symptom Scale.

176 .9]; P = .01; higher better) and Lee chronic graft-vs-host disease symptom scores (13.1 [1.5] vs 19.3

177 urrent paradigm, we find that, in a model of graft-vs-host disease, the immunotherapeutic effect of c

178 display antiviral activity without inducing graft-vs-host disease; therefore, we determined whether

179 imates were calculated for acute and chronic graft-vs-host disease, toxicities, achievement of full d

180 ine bone marrow (BM) NK T cells can suppress graft-vs-host disease, transplant rejection, and MLRs.

181 Graft vs. host disease was a predictor of a poor outcome

182 tioning regimen, and presence of significant graft vs. host disease was not found to influence outcom

183 y, severity, and pattern of tissue injury of graft-vs-host disease was assessed.

184 and mechanical ventilation; grade 3/4 acute graft-vs-host disease was associated with all-cause mort

185 a CD8(+) T cell adoptive transfer model for graft-vs-host disease, we demonstrate that a potent type

186 demonstrated in a parent-into-F(1) model of graft-vs-host disease, where dual TCR T cells comprised

187 lly irradiated wild-type B6 mice cause acute graft vs host disease with bone marrow failure.

188 revent and alter the course of a stimulatory graft-vs-host disease with a lupus-like syndrome.