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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

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