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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
30 ving RBC transfusions are at risk of forming alloantibodies against donor RBC antigens, and valid est
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
35 nsplantation nephritis, which is mediated by alloantibodies against the GBM, occurs after kidney tran
37 ytopenia (FNAIT) is often caused by maternal alloantibodies against the human platelet antigen (HPA)-
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
43 isease states, patient age, or the number of alloantibodies already formed, and only weakly dependent
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
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
56 heart grafts provoked strong germinal centre alloantibody and autoantibody responses in C57BL/6 recip
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
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
70 Antibody-mediated rejection triggered by alloantibody binding and complement activation is recogn
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.
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
79 erous studies demonstrate that anti-platelet alloantibodies can induce significant platelet clearance
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.
87 hat platelets recruit leukocytes to sites of alloantibody deposition and sustain leukocyte-endothelia
89 that lead to the formation of posttransplant alloantibodies despite immunosuppressive therapy have no
91 The development of sensitive methods for alloantibody detection has been a significant advance in
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
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.
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.
107 t a potential strategy to prevent anti-FVIII alloantibody formation in patients with hemophilia A.
109 s harbor molecular RH variants, which permit alloantibody formation to high-prevalence Rh antigens af
113 = 0.0001), and pretransplant panel reactive alloantibody >15% in either class I or class II (P = 0.0
115 ti-human leukocyte antigen (HLA) circulating alloantibodies in a cohort of 57 patients recruited at o
117 The unusually rapid appearance of de novo alloantibodies in immunosuppressed nonsensitized recipie
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
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
130 development of neutralizing anti-factor VIII alloantibodies (inhibitors) in patients with severe hemo
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
136 G1 (IL-4-dependent isotype) was the dominant alloantibody isotype in wild-type recipients as well as
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
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
149 elet removal in the absence of anti-platelet alloantibodies, many patients experience platelet cleara
151 disparities, cognate help for class-switched alloantibody may also be provided by CD4 T cells specifi
153 loantigens with 0 to 2 mismatched AA-induced alloantibody (median fluorescence intensity 37) compared
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
167 odies to polymorphic recipient antigens (ie, alloantibody) or nonpolymorphic antigens common to both
170 ned effects of functional memory B cells and alloantibodies prevent anti-CD154-mediated graft accepta
175 acept-treated animals demonstrated increased alloantibody production (100%) and morphologic features
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
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
187 l rejection in which CD4(+) T cell-dependent alloantibody production results in the targeting of tran
189 sA that achieved efficient B cell depletion, alloantibody production was substantially inhibited and
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
202 le antigens tested with monoclonal or eluted alloantibodies proved very powerful in identifying epito
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
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.
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
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
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
232 thway CD4 T cells developed long-lasting IgG alloantibody responses, with splenic GCs and allospecifi
239 ed on integrin beta3, is the main target for alloantibodies responsible for fetal and neonatal alloim
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
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
252 ransplant serum levels of a defined panel of alloantibodies targeting non-HLA immunogenic antigens as
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
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
264 nt nephritis mediated by pathogenic anti-GBM alloantibodies to collagen IV chains present in the rena
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
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
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-
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
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
291 rative inflammation subsided, donor-specific alloantibodies were passively transferred to the recipie
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
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
300 antation, with mounting evidence associating alloantibodies with the development of chronic rejection
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