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 development of swine MHC-specific cytotoxic alloantibody.

5 pment of posttransplant de novo HLA-specific alloantibodies.

6 lloantibodies as compared with those without alloantibodies.

7 No recipients produced donor-specific alloantibodies.

8 epitope and inhibits the binding of maternal alloantibodies.

9 allospecificity, leading to the induction of alloantibodies.

10 ero: shielding fetal platelets from maternal alloantibodies.

11 s become secondary targets of anti-alpha5NC1 alloantibodies.

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

13 transfusion recipients is the development of alloantibodies.

14 risk of occurrence of factor VIII inhibitory alloantibodies.

15 e time might deplete human leukocyte antigen-alloantibodies.

16 critical elements of epitopes recognized by alloantibodies.

17 ther chronic lesions or anti-HLA circulating alloantibodies.

18 fere with the detection of platelet-reactive alloantibodies.

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

20 utics aimed at pathogenic autoantibodies and alloantibodies.

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

22 and a risk of the development of inhibitory alloantibodies.

23 osition on HLA-coated microbeads spiked with alloantibodies.

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

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

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

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

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

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

30 Although alloantibodies against HLA antigens contribute to the pa

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

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

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

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

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

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

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

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

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

40 1 (2/9), completely attenuated IgM antidonor alloantibody (alloAb) production during treatment; 5C8H1

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

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

43 Non-HLA alloantibodies and autoantibodies are involved in allogr

44 Alloantibodies and B lymphocytes are felt to contribute

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

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

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

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

49 Levels of alloantibodies and SAP in the circulation were determine

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

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

52 0L blockade, but rejecting recipients lacked alloantibody and alloantigen-specific CD4 T-cell respons

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

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

55 Alloantibody and complement deposition on graft endothel

56 ery grafts in immunodeficient mouse hosts by alloantibody and complement similarly depends on assembl

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

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

59 the paratope-epitope relationship between an alloantibody and its target HLA molecule in a biological

60 ta, which lacks comprehensive information on alloantibody and rejection.

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

62 ly, strategies used to reduce donor-specific alloantibodies are collectively called desensitization.

63 It is estimated that only 30% of induced RBC alloantibodies are detected, given alloantibody inductio

64 Current methods to reduce alloantibodies are only modestly successful.

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

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

67 alleles that are bound strongly by the test alloantibody as opposed to those bound weakly and this p

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

69 with serial liver tests and autoantibody and alloantibody assessments.

70 with serial liver tests and autoantibody and alloantibody assessments.

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

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

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

74 ecules helps explain serological patterns of alloantibody binding.

75 mechanistic explanation for how fundamental alloantibody biology influences the readout from the SAB

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

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

78 Reliable detection of alloantibodies by immunoassays using alpha345NC1 hexamer

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

80 Alloantibodies can also be clinically significant in fut

81 Such alloantibodies can be generated by previous exposure to

82 As in HLA alloimmunity, donor-specific alloantibodies can be identified against genotype derive

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

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

85 Alloantibodies can play a key role in acute and chronic

86 Alloantibody can be a major barrier to successful organ

87 Alloantibody can contribute significantly to rejection o

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

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

90 We show that alloantibody concentration, subclass, laboratory-specifi

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

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

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

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

95 anescence patterns, missed opportunities for alloantibody detection, and record fragmentation.

96 Alloantibodies develop against the NC1 domain of alpha5(

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

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

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

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

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

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

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

104 the outcome of patients with donor specific alloantibody (DSA) at the time of transplantation and id

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

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

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

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

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

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

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

112 ter understanding of factors that impact RBC alloantibody formation may allow general or targeted pre

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

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

115 exhibit distinct propensities to induce RBC alloantibody formation.

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

117 = 0.0001), and pretransplant panel reactive alloantibody >15% in either class I or class II (P = 0.0

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

119 alloimmunity and as targets of nephritogenic alloantibodies in APTN.

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

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

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

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

124 28 blockade attracts interest for control of alloantibodies in the clinic, these data support selecti

125 Circulating alloantibodies in transplant recipients are often associ

126 assessing the occurrence and significance of alloantibodies in UET in reference to immunological para

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

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

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

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

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

132 duced RBC alloantibodies are detected, given alloantibody induction and evanescence patterns, missed

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

134 21 wild-type female mice developed anti-KEL alloantibodies; intrauterine fetal anemia and/or demise

135 The absence of alloantibodies is a feature of transplantation tolerance

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

137 f human leukocyte antigens (HLA) by anti-HLA alloantibodies is principally based upon in silico model

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

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

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

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

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

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

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

145 Alloantibody levels gradually declined but were still de

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

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

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

149 tization based on circulating donor-specific alloantibody levels.

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

151 Alloantibodies may be clinically significant in future t

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

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

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

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

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

157 8-deficient hosts to focus on CD4-dependent, alloantibody-mediated rejection.

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

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

160 ntibodies or Alport posttransplant nephritis alloantibodies mediating rapidly progressive glomerulone

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

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

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

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

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 difficult or impossible when autoantibodies, alloantibodies, or therapeutic antibodies coexist.

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

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 owing adoptive transfer into C57BL/6 or high alloantibody-producing CD8 knock out (KO) hepatocyte tra

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

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

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

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

179 alloprimed CXCR3CXCR5CD8 T cells) suppressed alloantibody production and enhanced graft survival when

180 ntragraft memory T cell expansion but not to alloantibody production and that a therapeutic strategy

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

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

183 cytotoxicity and capacity to inhibit in vivo alloantibody production following adoptive transfer into

184 subset significantly inhibits posttransplant alloantibody production in a murine transplant model.

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

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

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

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

189 Alloantibody production is dependent on T-cell help via

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

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

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

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

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

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

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

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

198 reported to promote graft rejection through alloantibody production.

199 med CD8 T cells that suppress posttransplant alloantibody production.

200 nal influenza does not result in significant alloantibody production.

201 4(+) T cells are critical for posttransplant alloantibody production.

202 rofile shifts the alloimmune response toward alloantibody production.

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 The durable alloantibody responses that develop in organ transplant

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

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

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

231 T cells recapitulated class-switched recall alloantibody responses.

232 derived mediators may be markers of evolving alloantibody responses.

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

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

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

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

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

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

243 ional characterization of a human monoclonal alloantibody specific for a common HLA type, HLA-A*11:01

244 Other alloantibodies specifically targeted alloepitopes that d

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

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

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

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

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

250 D8 T cells from CXCR5 KO mice do not develop alloantibody-suppressor function.

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

260 f clinically important and rare HPA-specific alloantibodies that, to date, have resisted detection us

261 Alloantibody titer was assessed in CD8 KO mice reconstit

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

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

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

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

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

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

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

269 Detection of alloantibodies to human platelet antigen 3 (HPA-3) and H

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

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

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

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

274 Alloantibodies to the Bw4 epitope are known to be hetero

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

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

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

278 fts is mediated by pathogenic donor-specific alloantibodies, usually of the IgG isotype.

279 Identification of alloantibodies was performed with the use of protein arr

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

281 HLA alloantibody was determined by Luminex single-antigen be

282 udy, a structurally-defined human monoclonal alloantibody was employed to provide a mechanistic expla

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

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

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

286 Sustained alloantibodies were detected in rejecting grafts and abs

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

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

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

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

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 Modification of alloimmunity and alloantibodies will also have relevance to xenotransplan

299 Thus, alloantibodies with restricted specificity are able to f

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