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 No graft succumbed to hyperacute rejection.

3 ible organ transplantation typically induces 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 onse to xenografts that are not subjected to hyperacute rejection.

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

9 component deposition and consumption during hyperacute rejection.

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

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

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

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

14 topes on the graft endothelium could prevent hyperacute rejection.

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

16 omerular thrombosis but no other evidence of hyperacute rejection.

17 he very early pathophysiologic events during hyperacute rejection.

18 from Lewis rats by antibody therapy prevents hyperacute rejection.

19 successful discordant xenotransplantation is hyperacute rejection.

20 ng xenotransplantation antigens resulting in hyperacute rejection.

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

22 All renal xenografts avoided hyperacute rejection.

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

24 some protection against complement-mediated hyperacute rejection.

25 renal transplantation because of the risk of hyperacute rejection.

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

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

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

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

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

31 on pig endothelium in the protection against hyperacute rejection.

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

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

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

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

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

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

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

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

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

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

42 0(8) nonparenchymal cells (NPC), resulted in hyperacute rejection and death in < or = 1.9 days.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

70 Hyperacute rejection does not occur in guinea pig cornea

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

72 No hyperacute rejection episodes occurred.

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

74 Hyperacute rejection (HAR) and acute humoral rejection (

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

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

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

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

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

80 Hyperacute rejection (HAR) is the first critical immunol

81 Hyperacute rejection (HAR) mediated by xenoreactive natu

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

109 Hyperacute rejection in xenotransplantation is caused by

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

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

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

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

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

115 When hyperacute rejection is averted, transplanted pig organs

116 When hyperacute rejection is avoided by deletion of Gal expre

117 Classic hyperacute rejection is dependent on the activation of t

118 To avoid hyperacute rejection it is essential that recipient anti

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

120 The hyperacute rejection mediated by preexisting antibodies

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

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

123 Hyperacute rejection occurred only in transplanted kidne

124 No hyperacute rejection occurred.

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

126 Hyperacute rejection of a porcine organ by higher primat

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

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

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

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

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

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

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

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

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

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

137 Hyperacute rejection of mouse lung by human blood occurs

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

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

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

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

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

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

144 Hyperacute rejection of porcine organs by old world prim

145 Hyperacute rejection of porcine organs transplanted into

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

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

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

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

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

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

152 Hyperacute rejection of solid organ pig xenografts in no

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

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

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

156 Hyperacute rejection of vascularized discordant xenograf

157 The hyperacute rejection of vascularized grafts exchanged be

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

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

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

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

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

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

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

165 Hyperacute rejection results from the deposition of pref

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

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

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

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

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

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

172 Hyperacute rejection, the initial and immediate barrier

173 Hyperacute rejection, the initial immune barrier to succ

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

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

176 The clinical diagnosis of hyperacute rejection was made.

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

178 No hyperacute rejection was observed.

179 No hyperacute rejection was seen and histologic findings we

180 Hyperacute rejection was uncommon.

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

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

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

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

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

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

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

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