ライフサイエンスコーパス: hyperacute rejection

1 cular injury due to immune damage (acute and hyperacute rejection).

2 e solid organ transplantation and preventing hyperacute rejection.

3 No graft succumbed to hyperacute rejection.

4 acute xenograft rejection was able to induce hyperacute rejection.

5 y of IgM to induce complement activation and hyperacute rejection.

6 esponse against xenografts in the absence of hyperacute rejection.

7 ible organ transplantation typically induces hyperacute rejection.

8 onse to xenografts that are not subjected to hyperacute rejection.

9 rn goats: none of these xenografts underwent hyperacute rejection.

10 component deposition and consumption during hyperacute rejection.

11 anges in anti-Gal activity in the absence of hyperacute rejection.

12 No graft was lost as a result of classic hyperacute rejection.

13 to evaluate the ability of hCD59 to inhibit hyperacute rejection.

14 d are liable to immediate graft loss through hyperacute rejection.

15 topes on the graft endothelium could prevent hyperacute rejection.

16 be of therapeutic value in the prevention of hyperacute rejection.

17 omerular thrombosis but no other evidence of hyperacute rejection.

18 he very early pathophysiologic events during hyperacute rejection.

19 from Lewis rats by antibody therapy prevents hyperacute rejection.

20 successful discordant xenotransplantation is hyperacute rejection.

21 course, such as primary graft dysfunction or hyperacute rejection.

22 ipient cytokine levels are not suggestive of hyperacute rejection.

23 xenotransplanted lung and the possibility of hyperacute rejection.

24 an recipients for 54 hours, without signs of hyperacute rejection.

25 The challenge in this model has been hyperacute rejection.

26 ng xenotransplantation antigens resulting in hyperacute rejection.

27 a high likelihood of success with respect to hyperacute rejection.

28 All renal xenografts avoided hyperacute rejection.

29 some protection against complement-mediated hyperacute rejection.

30 renal transplantation because of the risk of hyperacute rejection.

31 r-specific antibodies (DSAs) are culprits of hyperacute rejection.

32 ft and one patient lost her graft because of hyperacute rejection.

33 and continuing cyclosporin A (CyA) prevented hyperacute rejection.

34 s treated by cobra venom factor to avoid the hyperacute rejection.

35 elicited anti-donor IgM and IgG that caused hyperacute rejection.

36 ipients and is essential in the treatment of hyperacute rejection.

37 on pig endothelium in the protection against hyperacute rejection.

38 ot receive PP, lost her allograft because of hyperacute rejection.

39 i-A2 antibodies and for reducing the risk of hyperacute rejection.

40 ar endothelium of the graft, consistent with hyperacute rejection.

41 be divided temporally into three categories: hyperacute rejection, acute humoral rejection and chroni

42 antigen antibodies were then found to cause hyperacute rejection, acute rejection, and chronic rejec

43 Despite significant progress in overcoming hyperacute rejection, adaptive cellular and humoral immu

44 e diabetes but whether islets are subject to hyperacute rejection after xenotransplantation is conten

45 ation are surmounted, such as suppression of hyperacute rejection allowing improved graft survival, i

46 stological examination showed no evidence of hyperacute rejection, although deposits of IgG2a and C3

47 he role of antibodies is incontrovertible in hyperacute rejection, although what fraction of acute re

48 There were no episodes of hyperacute rejection and 1 episode of early antibody-med

49 r of ESRD patients have shown no evidence of hyperacute rejection and adequate pig kidney function fo

50 0(8) nonparenchymal cells (NPC), resulted in hyperacute rejection and death in < or = 1.9 days.

51 sfunction, with the potential to progress to hyperacute rejection and death.

52 lactose-alpha1,3-galactose epitope prevented hyperacute rejection and extended survival of pig hearts

53 an factor Xa inhibition by porcine EC during hyperacute rejection and loss of porcine EC TFPI during

54 pecific antibodies have been associated with hyperacute rejection and primary graft failure in lung t

55 gh the use of GalT-KO swine donors prevented hyperacute rejection and prolonged graft survival, slowl

56 Immediate pretransplant IA can prevent hyperacute rejection and provide an opportunity for succ

57 pients (median titer, 1:512), with 2 showing hyperacute rejection and rapid cessation of graft pulsat

58 studies in this patient are consistent with hyperacute rejection and support a pathogenic role of th

59 y, infants may have relative protection from hyperacute rejection and thus could undergo transplantat

60 , has substantially reduced the incidence of hyperacute rejection and, for years, has been the gold s

61 There were no hyperacute rejections and very infrequent acute rejectio

62 into baboons, the grafts did not succumb to hyperacute rejection, and survival extended for up to 23

63 No patient experienced hyperacute rejection, and the persistence of low levels

64 most striking immunologic obstacle, that of hyperacute rejection, appears to be the closest to being

65 The clinical and pathologic findings seen in hyperacute rejection are well documented in renal and ca

66 transgenic organs expressing hCD69 resisted hyperacute rejection, as measured by increased organ fun

67 None had hyperacute rejection but 11 (39%) had acute antibody med

68 arts transplanted into rats do not encounter hyperacute rejection but are rejected within 3-4 days wh

69 f complement receptor type 1 (sCR1) prevents hyperacute rejection but not subsequent irreversible acc

70 This conditioning regimen prevented hyperacute rejection but was ineffective in preventing t

71 Liver allografts rarely undergo hyperacute rejection, but transplants performed across a

72 was detected in pig control organs and after hyperacute rejection, but was lost from the vasculature

73 The recent advances in avoiding hyperacute rejection by producing transgenic pigs with c

74 Current data suggest that hyperacute rejection can be overcome in a clinically acc

75 In pig-to-primate organ transplantation, hyperacute rejection can be prevented, but the organ is

76 Unlike acute and hyperacute rejection, chronic rejection (CR) still const

77 The ability of serum to induce hyperacute rejection correlated with its ability to indu

78 Hyperacute rejection did not occur in alpha1,3-galactosy

79 We have previously demonstrated that hyperacute rejection does not occur in a pig-to-newborn

80 Hyperacute rejection does not occur in guinea pig cornea

81 Our study demonstrates that hyperacute rejection does not occur, allowing limited pr

82 drate antigens, posing significant risks for hyperacute rejection during ABO-incompatible transplanta

83 No hyperacute rejection episodes occurred.

84 cy of cobra venom factor (CVF) in preventing hyperacute rejection (HAR) after pig-to-baboon heart tra

85 Hyperacute rejection (HAR) and acute humoral rejection (

86 Xenografts that have been protected from hyperacute rejection (HAR) are termed accommodated if th

87 T) in the donor cell or tissue protects from hyperacute rejection (HAR) by reducing expression of Gal

88 regulatory proteins reduces the frequency of hyperacute rejection (HAR) in Gal-positive cardiac xenot

89 In the pig-to-primate model, xenograft hyperacute rejection (HAR) is mediated by antibody and c

90 layed xenograft rejection (DXR), occurs when hyperacute rejection (HAR) is prevented by strategies di

91 Hyperacute rejection (HAR) is the first critical immunol

92 Hyperacute rejection (HAR) mediated by xenoreactive natu

93 role of anti-Gal Abs and non-anti-Gal Abs in hyperacute rejection (HAR) of concordant pancreas xenogr

94 tibodies) are the primary effectors of human hyperacute rejection (HAR) of nonhuman tissue.

95 Hyperacute rejection (HAR) of pig-to-primate discordant

96 type 1 (sCR1, TP-10) has been shown to delay hyperacute rejection (HAR) of porcine cardiac xenografts

97 for clinical xenograft transplantation, and hyperacute rejection (HAR) or acute humoral xenograft re

98 e to graft dysfunction during development of hyperacute rejection (HAR), as well as during what we ha

99 owed minimal evidence of complement-mediated hyperacute rejection (HAR), but prominent mononuclear ce

100 ans are rapidly rejected by a process called hyperacute rejection (HAR), there is hope that several n

101 Abs mediate a classical complement-dependent hyperacute rejection (HAR), while anti-Gal IgG1 mAbs med

102 /kg) as a single dose to evaluate effects on hyperacute rejection (HAR).

103 (PVR), which is a characteristic feature of hyperacute rejection (HAR).

104 membrane attack complex (C5b-9) in mediating hyperacute rejection has been demonstrated previously in

105 Significant advances in controlling hyperacute rejection have been achieved recently through

106 onal immunosuppression is unable to overcome hyperacute rejection; however, recent efforts in molecul

107 tion of the immediate pathologic features of hyperacute rejection in a lung allograft which are simil

108 We describe the second case of hyperacute rejection in a pulmonary allograft and detail

109 third case and first successful treatment of hyperacute rejection in a pulmonary allograft recipient

110 ement regulatory proteins (CRPs) can prevent hyperacute rejection in discordant xenogenic recipients,

111 The expression of DAF prevents hyperacute rejection in mice with low titers of anti-alp

112 R), which are the major xenoantigens causing hyperacute rejection in pig-to-human xenotransplantation

113 lpha1,3Gal) is the major xenoantigen causing hyperacute rejection in pig-to-human xenotransplantation

114 suitable potential donor species, results in hyperacute rejection in primate recipients, due to the p

115 ccommodation of IEC may confer resistance to hyperacute rejection in sensitized recipients.

116 There was no evidence of hyperacute rejection in six of the nine patients; the ot

117 There was no hyperacute rejection in the immediate postoperative phas

118 To address the pathogenesis of hyperacute rejection in the pig-to-human combination, F1

119 ositive, CXM negative, but no grafts lost to hyperacute rejection in this group.

120 on by a process that has features similar to hyperacute rejection in vascularized organs and we propo

121 etermine whether sensitization would lead to hyperacute rejection in VCTA as in other organs, such as

122 Hyperacute rejection in xenotransplantation is caused by

123 veloped to help overcome complement-mediated hyperacute rejection in xenotransplantation.

124 dence for complement activation in xenograft hyperacute rejection includes prolongation of graft surv

125 a pig organ is transplanted into a primate, hyperacute rejection, induced by anti-pig antibody and m

126 ions are designed to reduce or eliminate the hyperacute rejection inherent in pig-to-primate xenotran

127 However, when hyperacute rejection is averted, the xenografts are reje

128 When hyperacute rejection is averted, transplanted pig organs

129 When hyperacute rejection is avoided by deletion of Gal expre

130 Classic hyperacute rejection is dependent on the activation of t

131 To avoid hyperacute rejection it is essential that recipient anti

132 le to cross-species transplantation has been hyperacute rejection mediated by complement fixing antib

133 The hyperacute rejection mediated by preexisting antibodies

134 on; however, none has been shown to manifest hyperacute rejection mediated by the classical pathway o

135 olyreactive, a new prophylactic strategy for hyperacute rejection might be based on down-regulation o

136 Hyperacute rejection occurred only in transplanted kidne

137 No hyperacute rejection occurred.

138 t's anti-alphaGal profile, (2) prevention of hyperacute rejection of a pig organ, and (3) specific im

139 Hyperacute rejection of a porcine organ by higher primat

140 strate that C5b-9 plays an important role in hyperacute rejection of a porcine organ perfused with hu

141 recipient HLA-specific antibodies can cause hyperacute rejection of a transplanted kidney if they ar

142 almost certainly be sufficient to delay the hyperacute rejection of a transplanted pig organ, but fu

143 lusion resulting in infarction occurs during hyperacute rejection of allografts transplanted into sen

144 ciation of preformed anti-donor Abs with the hyperacute rejection of bone marrow and solid organ allo

145 ral antibodies (XNAs) and complement mediate hyperacute rejection of discordant xenografts.

146 dergo delayed rejection as compared with the hyperacute rejection of discordant xenografts.

147 n anti-GAL antibodies and are able to induce hyperacute rejection of GAL+ heart allografts.

148 donor-specific sensitization would result in hyperacute rejection of IECs and prevent islet engraftme

149 whether accommodation of IECs would prevent hyperacute rejection of islets in sensitized recipients.

150 Hyperacute rejection of mouse lung by human blood occurs

151 sitization against donor antigens results in hyperacute rejection of murine islets.

152 ajor role of anti-alphaGal antibodies in the hyperacute rejection of pig organs by humans and baboons

153 l (alphaGal) natural antibodies leads to the hyperacute rejection of pig organs transplanted into pri

154 lphaGal) antibodies can prevent or delay the hyperacute rejection of pig organs transplanted into pri

155 n by human blood ex vivo, a working model of hyperacute rejection of porcine by fresh, heparinized (6

156 motif is the primary contributing factor in hyperacute rejection of porcine organ xenograft, due to

157 Hyperacute rejection of porcine organs by old world prim

158 Hyperacute rejection of porcine organs transplanted into

159 Although preformed natural antibodies cause hyperacute rejection of primarily vascularized xenograft

160 embrane-bound complement regulation to blunt hyperacute rejection of pulmonary xenografts, but even t

161 e therapy, whereas delayed vascular and even hyperacute rejection of rat hearts occurred in condition

162 The same process results in hyperacute rejection of renal allografts transplanted in

163 antibodies to HLA class I antigens can cause hyperacute rejection of renal allografts.

164 ew model enabling serial biopsies of ongoing hyperacute rejection of small intestinal discordant xeno

165 Hyperacute rejection of solid organ pig xenografts in no

166 , but not third-party, sensitization induced hyperacute rejection of subsequent islet allografts (med

167 a series of violent reactions that result in hyperacute rejection of the xenograft.

168 ing factor (hCRF) in porcine organs prevents hyperacute rejection of these organs after xenotransplan

169 Hyperacute rejection of vascularized discordant xenograf

170 The hyperacute rejection of vascularized grafts exchanged be

171 ion may be beneficial to patients undergoing hyperacute rejection of xenografts or allografts.

172 The results may have relevance to hyperacute rejection of xenografts, as from pigs to prim

173 ress human CD59 (hCD59) in order to suppress hyperacute rejection of xenotransplants in human recipie

174 mplement-fixing IgG3 mAbs resulted in either hyperacute rejection or acute vascular rejection of the

175 s of the monitoring period, without signs of hyperacute rejection or infection.

176 tation can be performed successfully without hyperacute rejection or zoonosis.

177 ssion regimen was immediately modified and a hyperacute rejection protocol applied including plasmaph

178 nkeys after column perfusion did not undergo hyperacute rejection, remaining functional for 2-10 days

179 tissues usually results in antibody-mediated hyperacute rejection response.

180 Hyperacute rejection results from the deposition of pref

181 est that sublytic deposition of C5b-9 during hyperacute rejection results in the expression of porcin

182 transgenic pigs may overcome the barrier of hyperacute rejection, special strategies will need to be

183 mulated T cells were relatively resistant to hyperacute rejection, suggesting an explanation for the

184 nd may therefore be of use in preventing the hyperacute rejection that follows discordant organ xenot

185 trast, an anti-Gal IgG3 mAb induced classic, hyperacute rejection that was solely dependent on comple

186 In the absence of complement-mediated hyperacute rejection, the ADCC induced by anti-Gal IgG m

187 Hyperacute rejection, the initial and immediate barrier

188 Hyperacute rejection, the initial immune barrier to succ

189 as being a major xenoantigen responsible for hyperacute rejection, the removal of anti-alphaGal antib

190 regulate complement activation and overcome hyperacute rejection upon transplantation of a vasculari

191 The clinical diagnosis of hyperacute rejection was made.

192 Hyperacute rejection was observed in 8/8 A-Tg grafts aft

193 No hyperacute rejection was observed, and the kidneys remai

194 No hyperacute rejection was observed.

195 No hyperacute rejection was seen and histologic findings we

196 Hyperacute rejection was uncommon.

197 Using a rat model of hyperacute rejection, we investigated the potential of o

198 No instances of hyperacute rejection were observed, and no grafts were l

199 e accommodated islets were resistant against hyperacute rejection when transplanted into donor-(splen

200 ajor obstacle to this xenotransplantation is hyperacute rejection, which is believed to be initiated

201 unological barrier to xenotransplantation is hyperacute rejection, which is mediated by xenoreactive

202 e conditions, nontransgenic grafts underwent hyperacute rejection within 90 min.

203 ition by human natural antibodies results in hyperacute rejection would allow for the development of

204 nograft model to examine our hypothesis that hyperacute rejection would be absent in newborn recipien