ライフサイエンスコーパス: alloantibody

1 te, altered Th1 responses, and reduced serum alloantibody.

2 gnition and the generation of donor specific alloantibody.

3 ckout mice do not produce any posttransplant alloantibody.

4 commonly confirmed by tests for circulating alloantibody.

5 ion (MLR) and flow cytometry to detect serum alloantibody.

6 development of swine MHC-specific cytotoxic alloantibody.

7 No recipients produced donor-specific alloantibodies.

8 epitope and inhibits the binding of maternal alloantibodies.

9 eactions, not all patients generate anti-RBC alloantibodies.

10 allospecificity, leading to the induction of alloantibodies.

11 ero: shielding fetal platelets from maternal alloantibodies.

12 s become secondary targets of anti-alpha5NC1 alloantibodies.

13 struction is mediated via the Fc part of the alloantibodies.

14 risk of occurrence of factor VIII inhibitory alloantibodies.

15 and a risk of the development of inhibitory alloantibodies.

16 e time might deplete human leukocyte antigen-alloantibodies.

17 osition on HLA-coated microbeads spiked with alloantibodies.

18 BCs bearing low Ag levels fail to induce RBC alloantibodies.

19 critical elements of epitopes recognized by alloantibodies.

20 ther chronic lesions or anti-HLA circulating alloantibodies.

21 emophilia A or B who did not have inhibitory alloantibodies.

22 ctor for the development of anti-factor VIII alloantibodies.

23 emophilia A or B who did not have inhibitory alloantibodies.

24 nce in the complete absence of anti-platelet alloantibodies.

25 pment of posttransplant de novo HLA-specific alloantibodies.

26 lloantibodies as compared with those without alloantibodies.

27 the incidence of clinically significant RBC alloantibodies (abs) in 2000 consecutive adults receivin

28 Alloantibodies absorbed onto then eluted from HLA single

29 hose without nephritis, produce two kinds of alloantibodies against allogeneic collagen IV.

30 ving RBC transfusions are at risk of forming alloantibodies against donor RBC antigens, and valid est

31 Although alloantibodies against HLA antigens contribute to the pa

32 andard for immunotyping sera with respect to alloantibodies against human platelet antigens (HPA).

33 igens contribute to the pathogenesis of CAI, alloantibodies against non-HLA antigens likely contribut

34 During RBC transfusion, production of alloantibodies against RBC non-ABO Ags can cause hemolyt

35 nsplantation nephritis, which is mediated by alloantibodies against the GBM, occurs after kidney tran

36 Maternal alloantibodies against the human platelet Ag (HPA)-1a al

37 ytopenia (FNAIT) is often caused by maternal alloantibodies against the human platelet antigen (HPA)-

38 sensitized kidney transplant candidates with alloantibodies against their intended living donor.

39 The development of alloantibodies against von Willebrand factor (VWF) repre

40 tains approximately 94% fucosylated Abs, but alloantibodies against, for example, Rhesus D (RhD) and

41 1 (2/9), completely attenuated IgM antidonor alloantibody (alloAb) production during treatment; 5C8H1

42 ens resulted in the development of antidonor alloantibody (alloAb) with accelerated kinetics.

43 isease states, patient age, or the number of alloantibodies already formed, and only weakly dependent

44 Non-HLA alloantibodies and autoantibodies are involved in allogr

45 Alloantibodies and B lymphocytes are felt to contribute

46 th isotype and specificity of donor-reactive alloantibodies and can thus affect allograft pathology.

47 ers, as well as production of donor-specific alloantibodies and complement deposition in the transpla

48 t risk for de novo development of pathogenic alloantibodies and for preventing alloantibody productio

49 The presence of alloantibodies and high plasma B cell-activating factor

50 Levels of alloantibodies and SAP in the circulation were determine

51 nied by higher levels of circulating IgM/IgG alloantibodies and SAP than in WT recipients.

52 vealed increased development of HLA class II alloantibodies and Th1-predominant donor-specific cellul

53 ell antibodies were seen in six patients (11 alloantibodies and two autoantibodies), among whom three

54 0L blockade, but rejecting recipients lacked alloantibody and alloantigen-specific CD4 T-cell respons

55 therapeutic approaches aimed at controlling alloantibody and assess their efficacy.

56 heart grafts provoked strong germinal centre alloantibody and autoantibody responses in C57BL/6 recip

57 Alloantibody and complement deposition on graft endothel

58 mTORi and/or CNi and serially monitored for alloantibody and graft survival.

59 elp fails to maintain stable levels of serum alloantibody and induce differentiation of long-lived pl

60 Furthermore, hepatocyte coincubation with alloantibody and macrophages resulted in Ab-dependent he

61 Recipients produced alloantibody and showed luminal occlusion at 1 (17.7%+/-

62 The causal relationship between alloantibody and transplant rejection-especially chronic

63 eous, but it is widely assumed that anti-Bw4 alloantibodies arise only in individuals who do not expr

64 in chronically transfused SCD patients with alloantibodies as compared with those without alloantibo

65 donor-specific anti-human leukocyte antigen alloantibody, as determined retrospectively, suggesting

66 with serial liver tests and autoantibody and alloantibody assessments.

67 with serial liver tests and autoantibody and alloantibody assessments.

68 is relatively ineffective in preventing late alloantibody-associated chronic rejection.

69 Adding the presence of donor-specific alloantibody at 1 year did not improve predictability or

70 Antibody-mediated rejection triggered by alloantibody binding and complement activation is recogn

71 ecules helps explain serological patterns of alloantibody binding.

72 ith Alport's post-transplantation nephritis, alloantibodies bound to the E(A) region of the alpha5NC1

73 wo of 30 vaccinated volunteers developed new alloantibodies, but none of the transplant patients.

74 Reliable detection of alloantibodies by immunoassays using alpha345NC1 hexamer

75 s examining correlations between circulating alloantibodies, C4d deposition, and rejection in lung tr

76 ociated with an increased incidence of serum alloantibody, C4d deposition and antibody-mediated rejec

77 Such alloantibodies can be generated by previous exposure to

78 Autoantibodies and alloantibodies can damage self-tissue or transplanted ti

79 erous studies demonstrate that anti-platelet alloantibodies can induce significant platelet clearance

80 Alloantibodies can play a key role in acute and chronic

81 Alloantibody can be a major barrier to successful organ

82 Alloantibody can contribute significantly to rejection o

83 It is now clear that alloantibody can, in concert with colony-stimulating fac

84 ssue of Blood, Arthur et al uncover that HLA alloantibodies cannot solely account for the immune mech

85 lure more than doubled in recipients who had alloantibodies compared with antibody-free patients.

86 Notch ligand blockade also dampened alloantibody deposition and prevented chronic rejection

87 hat platelets recruit leukocytes to sites of alloantibody deposition and sustain leukocyte-endothelia

88 T cells and B220(+) B-cell infiltration and alloantibody deposition.

89 that lead to the formation of posttransplant alloantibodies despite immunosuppressive therapy have no

90 ith cellular rejection and are distinct from alloantibodies detected using lymphocytes.

91 The development of sensitive methods for alloantibody detection has been a significant advance in

92 Alloantibodies develop against the NC1 domain of alpha5(

93 De novo alloantibodies (donor-specific antibody) contribute to a

94 In the alloantibody-driven cGVHD model, ibrutinib treatment res

95 g T cell-driven sclerodermatous cGVHD and an alloantibody-driven multiorgan system cGVHD model that i

96 lograft loss in patients with donor-specific alloantibodies (DSA) mean florescence intensity (MFI) gr

97 Donor-specific alloantibodies (DSA) mediate hyperacute and acute antibo

98 ansporter type 8 antigen) and donor-specific alloantibodies (DSA) were quantified.

99 with preformed or de novo HLA donor-specific alloantibodies (DSA).

100 ever, the primary location of donor-specific alloantibody (DSA)-producing cells after transplantation

101 ng lists, and the presence of donor-specific alloantibodies (DSAs) at the time of transplantation lea

102 ated not only acute graft rejection but also alloantibody elaboration and chronic graft rejection.

103 We tested the hypothesis that alloantibodies facilitate cellular rejection by function

104 llograft rejection, recipient leukocytes and alloantibodies first target donor endothelial cells.

105 n IL-14 transcript levels may play a role in alloantibody formation after renal transplantation.

106 tein, prevents renal allograft rejection and alloantibody formation in nonhuman primates.

107 t a potential strategy to prevent anti-FVIII alloantibody formation in patients with hemophilia A.

108 One variable that may influence alloantibody formation is RBC alloantigen density.

109 s harbor molecular RH variants, which permit alloantibody formation to high-prevalence Rh antigens af

110 Although B-cell depletion prevents alloantibody formation, nonhumoral functions of B cells

111 exhibit distinct propensities to induce RBC alloantibody formation.

112 However, B cell depletion inhibited alloantibody generation and significantly extended allog

113 = 0.0001), and pretransplant panel reactive alloantibody >15% in either class I or class II (P = 0.0

114 Anti-MHC class I alloantibodies have been implicated in the process of ac

115 ti-human leukocyte antigen (HLA) circulating alloantibodies in a cohort of 57 patients recruited at o

116 alloimmunity and as targets of nephritogenic alloantibodies in APTN.

117 The unusually rapid appearance of de novo alloantibodies in immunosuppressed nonsensitized recipie

118 There were no increases in HLA alloantibodies in patients who received adjuvanted vacci

119 er help to B cells and induce pathogenic IgG alloantibodies in the absence of CD40-CD154 interactions

120 patients who have donor-specific ABO or HLA alloantibodies in the absence of damage to their allogra

121 ffect of riboflavin to reduce donor-reactive alloantibodies in this chronic model.

122 Circulating alloantibodies in transplant recipients are often associ

123 As such, it is important to test for alloantibody in cases of morphological TCMR to optimize

124 A possible role for alloantibody in endothelial dysfunction is discussed.

125 deficient recipients, although the amount of alloantibody in the latter group was substantially highe

126 viding help to generate new specificities of alloantibody in transplant patients receiving immunosupp

127 B lymphocytes-and their secretory products, alloantibodies-in the pathogenesis of allograft rejectio

128 monstrate using a skin transplant model that alloantibody indirectly induces platelet activation and

129 onstrates an important role for platelets in alloantibody induced transplant rejection.

130 development of neutralizing anti-factor VIII alloantibodies (inhibitors) in patients with severe hemo

131 Repeated IgG2a alloantibody injections result in sustained platelet-end

132 21 wild-type female mice developed anti-KEL alloantibodies; intrauterine fetal anemia and/or demise

133 helium as well as the coincident presence of alloantibodies is consistent with previous findings in a

134 ty to provide help for generating long-lived alloantibody is likely one of the main mechanisms respon

135 In contrast, alloantibody is readily detected in CNi-treated recipien

136 G1 (IL-4-dependent isotype) was the dominant alloantibody isotype in wild-type recipients as well as

137 To investigate this possibility, alloantibody isotype profiles were examined in CD8-defic

138 fficient to induce high levels of pathogenic alloantibody, it does not sustain long-lasting anti-dono

139 igen loss,' in which antigen crosslinking by alloantibody leads to antigen removal rather than red bl

140 We studied circulating alloantibody levels and C4d deposition in two rat models

141 Host serum alloantibody levels correlated with in vivo allospecific

142 Alloantibody levels gradually declined but were still de

143 based on the observation that posttransplant alloantibody levels in CD8-deficient murine hepatocyte t

144 D8-depleted IL-4 knockout mice restores high alloantibody levels observed in CD8-depleted wild-type r

145 ction by stimulated T cells, and circulating alloantibody levels were determined by flow cytometry, u

146 D4 and CD8 T cells, transiently reduce serum alloantibody levels, and extend graft survival.

147 tization based on circulating donor-specific alloantibody levels.

148 Allograft-eluted alloantibodies mainly targeted two conformational alloep

149 elet removal in the absence of anti-platelet alloantibodies, many patients experience platelet cleara

150 Donor-specific HLA alloantibodies may cause acute and chronic antibody-medi

151 disparities, cognate help for class-switched alloantibody may also be provided by CD4 T cells specifi

152 Also, recent studies suggest that alloantibody may be upregulated due to vaccination.

153 loantigens with 0 to 2 mismatched AA-induced alloantibody (median fluorescence intensity 37) compared

154 , in large part due to chronic and insidious alloantibody-mediated graft injury.

155 8-deficient hosts to focus on CD4-dependent, alloantibody-mediated rejection.

156 transplant vasculopathy and, in particular, alloantibody-mediated transplant rejection.

157 In support, in a model of alloantibody-mediated vasculopathy, depletion of NK cell

158 ulprit alloantigen and primary target of all alloantibodies mediating APTN, whereas alpha1256NC1 hexa

159 ntibodies or Alport posttransplant nephritis alloantibodies mediating rapidly progressive glomerulone

160 levels, high serum titers of donor-specific alloantibody, minimal T cell infiltration, and intense C

161 eukocyte antigen (HLA)-DQ has emerged as the alloantibody most frequently associated with the generat

162 ing data collected on clinically significant alloantibodies (n = 452) in a male patient population.

163 aft survival, indicating that donor-specific alloantibodies (not T cells) were the critical effector

164 e-scale prospective studies on the effect of alloantibodies on graft survival showed that rates of gr

165 The impact of memory B cells and alloantibodies on the ability to induce transplantation

166 The development of alloantibodies or inhibitors is the most serious complic

167 odies to polymorphic recipient antigens (ie, alloantibody) or nonpolymorphic antigens common to both

168 Repeated transfers of alloantibodies over 1 week sustained high levels of plat

169 important to test transplant recipients for alloantibody post-transplantation?

170 ned effects of functional memory B cells and alloantibodies prevent anti-CD154-mediated graft accepta

171 Costimulatory blockade abrogated alloantibody produced through naive Th cell recognition

172 delayed graft rejection in both low and high alloantibody producers.

173 Donor specific alloantibody producing plasma cells (DSA-PCs) appear res

174 the generation, maintenance and survival of alloantibody-producing plasma cells.

175 acept-treated animals demonstrated increased alloantibody production (100%) and morphologic features

176 uppression of CD8 T cells which downregulate alloantibody production (CD8 TAb-supp cells).

177 ed periods posttransplantation and result in alloantibody production and chronic rejection of kidney

178 odalities are needed to eliminate or curtail alloantibody production and its deleterious effects on t

179 No relationship was found between alloantibody production and these changes.

180 n transplant recipients, directly suppressed alloantibody production by alloprimed IgG1 B cells and d

181 fic direct and indirect T cell responses and alloantibody production in monkeys (n = 5) that did not

182 pathogenic alloantibodies and for preventing alloantibody production in T cell-sensitized recipients.

183 precise mechanisms contributing to enhanced alloantibody production in the absence of CD8(+) T cells

184 f rapamycin inhibitors, but not CNi, reduced alloantibody production in transplant recipients, direct

185 Alloantibody production is dependent on T-cell help via

186 is CD8-mediated regulation of posttransplant alloantibody production is IFN-gamma-dependent.

187 l rejection in which CD4(+) T cell-dependent alloantibody production results in the targeting of tran

188 Strain-specific serology and HLA alloantibody production was determined pre- and postimmu

189 sA that achieved efficient B cell depletion, alloantibody production was substantially inhibited and

190 Early and consistent de novo alloantibody production with associated histological cha

191 migrate to the allograft and are involved in alloantibody production within a tertiary lymphoid organ

192 cytotoxicity against alloantigen, increased alloantibody production, and a decline in peripheral and

193 mmunogenic and induce enhanced inflammation, alloantibody production, and complement activation leadi

194 herapy, CMPD 167 with cyclosporine A delayed alloantibody production, suppressed cardiac allograft va

195 nal influenza does not result in significant alloantibody production.

196 4(+) T cells are critical for posttransplant alloantibody production.

197 rofile shifts the alloimmune response toward alloantibody production.

198 in vivo allocytotoxicity without influencing alloantibody production.

199 matched mouse heart grafts and inhibition of alloantibody production.

200 at was associated with a total inhibition of alloantibody production.

201 reported to promote graft rejection through alloantibody production.

202 le antigens tested with monoclonal or eluted alloantibodies proved very powerful in identifying epito

203 ABO and human leukocyte antigen (HLA) alloantibodies provide major immunologic barriers to suc

204 rimary CD4 TFH cell response nor an enhanced alloantibody reaction.

205 er there is evidence of tissue or peripheral alloantibody reactivity.

206 es to evaluate the efficacy of antiYIL-6R on alloantibody recall responses and to examine the impact

207 indicate that antiYIL-6R therapy attenuates alloantibody recall responses by modulating a number of

208 e with an antiYIL-6R monoclonal (mMR16-1) in alloantibody recall responses.

209 a and autoimmune disease, and contributes to alloantibody reduction in transplantation across immunol

210 mismatch scores also correlated closely with alloantibody response (P<0.001), but neither variable ha

211 e to anti-CD45RB mediated suppression of the alloantibody response and transplant tolerance induction

212 s of class II alloantigen immunogenicity and alloantibody response before kidney transplantation.

213 de (indirect pathway) and then assessing the alloantibody response to a heart graft.

214 compartment failed to mount a donor-specific alloantibody response to an organ transplant--despite un

215 opment of autoantibody, amplification of the alloantibody response, and rapid allograft rejection.

216 tacrolimus promotes a CD4+memory T cell and alloantibody response, with morphologic changes reflecti

217 rt in its capacity to form a BALB/c-specific alloantibody response.

218 RBC antigens can lead to an enhanced primary alloantibody response.

219 ignificantly decreased but did not eliminate alloantibody responses (IgG mean fluorescence intensity,

220 01, odds ratio 3.85 per AA) and magnitude of alloantibody responses (P<0.001); only 6% of alloantigen

221 t or 3 weeks later abrogated germinal centre alloantibody responses and blocked development of allogr

222 tive memory helper T cells can induce potent alloantibody responses and often associate with poor gra

223 ained disease free in B6 mice, much stronger alloantibody responses and progressive graft arteriopath

224 es that enable inhibition of germinal center alloantibody responses hold particular appeal.

225 CD4 T cell help for GC alloantibody responses is provided exclusively via the i

226 Essential help for long-lived alloantibody responses is theoretically provided only by

227 In contrast, the restoration of alloantibody responses required both the deletion of CD2

228 The durable alloantibody responses that develop in organ transplant

229 No indirect alloresponse by T cells and no alloantibody responses were found in any of the tolerant

230 developed only minimal vasculopathy, and the alloantibody responses were weaker, without observable a

231 me human transfusion recipients mount strong alloantibody responses, whereas others do not.

232 thway CD4 T cells developed long-lasting IgG alloantibody responses, with splenic GCs and allospecifi

233 ts as wild type recipients, with similar IgG alloantibody responses.

234 ype and CCR5(-/-) mice that have exaggerated alloantibody responses.

235 riables with the occurrence and magnitude of alloantibody responses.

236 emory B cells that are central to the recall alloantibody responses.

237 T cells recapitulated class-switched recall alloantibody responses.

238 derived mediators may be markers of evolving alloantibody responses.

239 ed on integrin beta3, is the main target for alloantibodies responsible for fetal and neonatal alloim

240 btained from mice incapable of secreting IgG alloantibody resulted in less BO and cGVHD.

241 identify metabolically active cells such as alloantibody secreting plasma cells.

242 Nevertheless, the numbers of alloantibody-secreting cells and the serum titers of ant

243 We conclude that cGVHD is caused in part by alloantibody secretion, which is associated with fibrosi

244 hrectomy and was an independent predictor of alloantibody sensitization after kidney allograft failur

245 Other alloantibodies specifically targeted alloepitopes that d

246 veillance biopsy and/or serum donor-specific alloantibody status could improve predictability of graf

247 ulopathy in the absence of other T cells and alloantibodies, suggesting a role for the direct pathway

248 ce and humans with no detectable circulating alloantibodies, suggesting that antibody-independent pat

249 trexate administration significantly reduced alloantibodies, suggesting that methotrexate not only de

250 ases, there were no other donor-specific HLA alloantibodies, suggesting that the HLA-DP-specific anti

251 Some alloantibodies targeted alloepitopes within alpha5NC1 mo

252 ransplant serum levels of a defined panel of alloantibodies targeting non-HLA immunogenic antigens as

253 Although definitive approaches to alloantibody testing are not possible with our current k

254 dual spleen ASCs produced more antidonor IgG alloantibody than bone marrow ASCs.

255 derived ECPs allow for the identification of alloantibodies that are associated with cellular rejecti

256 icient B cells and induce high titers of IgG alloantibodies that contribute to heart allograft reject

257 on can result in the development of anti-RBC alloantibodies that increase the probability of life-thr

258 replacement therapy after the development of alloantibodies that inhibit factor VIII (FVIII) activity

259 ents with hemophilia A is the development of alloantibodies that inhibit factor VIII activity.

260 s established by analysis of lymphocytotoxic alloantibodies that were made by pregnant women, directe

261 alpha345(IV) collagen promotes production of alloantibodies to alpha345NC1 hexamers, including proinf

262 Both kidney-eluted and circulating alloantibodies to alpha5NC1 distinctively targeted epito

263 Given that alloantibodies to antigens in the KEL family are among t

264 nt nephritis mediated by pathogenic anti-GBM alloantibodies to collagen IV chains present in the rena

265 o prevent and/or mitigate the dangers of RBC alloantibodies to fetuses and newborns.

266 ansfusion recipients fail to make detectable alloantibodies to foreign RBC antigens ("nonresponders")

267 These observations highlight the ability of alloantibodies to function not only in classical humoral

268 for patients with hemophilia A, neutralizing alloantibodies to FVIII, known as inhibitors, develop in

269 Alloantibodies to HLA class I or II and other antigens e

270 gimen in which more than 50% of mice develop alloantibodies to human glycophorin A antigen, we found

271 the potential ability of memory B cells and alloantibodies to prevent anti-CD154-mediated graft acce

272 and the subsequent transmission of maternal alloantibodies to pups through breast milk induces a pos

273 ific, because nonresponders to hGPA produced alloantibodies to RBCs that expressed a different transg

274 sponders were prone to developing additional alloantibodies to strong immunogens, whereas nonresponde

275 Alloantibodies to the Bw4 epitope are known to be hetero

276 ients tested at 0, 15, and 90 days presented alloantibodies to the UC-MSCs (n=7).

277 valuate the effects of K9.361, a mouse IgG2a alloantibody to mouse FcgammaRIIB, on murine anaphylaxis

278 demonstrate that BIVV009 effectively blocks alloantibody-triggered CP activation, even though short-

279 The presence of circulating donor-specific alloantibodies was verified by flow cytometry.

280 Alloantibody was assessed at 2, 4, and 8 weeks.

281 HLA alloantibody was determined by Luminex single-antigen be

282 In contrast, IgG alloantibody was not detectable in recipient mice recons

283 thod to identify persons most likely to make alloantibodies were available, this would not of itself

284 In fact, for nearly 50 years, anti-platelet alloantibodies were considered to be the sole mediator o

285 Sustained alloantibodies were detected in rejecting grafts and abs

286 nsfusion setting, and transfusion-associated alloantibodies were detrimental in a pregnancy setting.

287 observations in humans, pregnancy-associated alloantibodies were detrimental in a transfusion setting

288 Circulating donor-specific IgG alloantibodies were initially reduced with WT FR70 treat

289 ride binding protein (LBP) plasma as well as alloantibodies were measured simultaneously.

290 In vitro assays for alloantibodies were negative, and Elispots assays failed

291 rative inflammation subsided, donor-specific alloantibodies were passively transferred to the recipie

292 ntigen-specific responses and donor-specific alloantibody were also determined.

293 cells and the serum titers of antidonor IgG alloantibody were equivalent in sensitized and nonsensit

294 nergistic effects of memory 3-83 B cells and alloantibodies, whereas memory T cells are not necessary

295 Alport alloantibodies, which bound to native murine alpha3alpha

296 skin grafts and hence the generation of IgG alloantibodies, which depends on indirectly activated T

297 ic KEL2 RBCs generated anti-KEL glycoprotein alloantibodies, which fixed complement, led to intravasc

298 ysis demonstrated high levels of circulating alloantibodies with broad cross-reactivity to many MHC h

299 Thus, alloantibodies with restricted specificity are able to f

300 antation, with mounting evidence associating alloantibodies with the development of chronic rejection