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2 idney transplant recipients without anti-HLA donor-specific Abs who experienced acute graft dysfuncti
3 ath-censored allograft loss in patients with donor-specific alloantibodies (DSA) mean florescence int
5 idates on waiting lists, and the presence of donor-specific alloantibodies (DSAs) at the time of tran
6 extended allograft survival, indicating that donor-specific alloantibodies (not T cells) were the cri
7 lasmablast numbers, as well as production of donor-specific alloantibodies and complement deposition
10 After perioperative inflammation subsided, donor-specific alloantibodies were passively transferred
11 jury to allografts is mediated by pathogenic donor-specific alloantibodies, usually of the IgG isotyp
12 rder to predict the outcome of patients with donor specific alloantibody (DSA) at the time of transpl
14 s at 1-year surveillance biopsy and/or serum donor-specific alloantibody status could improve predict
15 erum creatinine levels, high serum titers of donor-specific alloantibody, minimal T cell infiltration
18 lopment of interstitial fibrosis and de novo donor specific anti-HLA antibodies (dnDSA) at 1 year.
20 until April 2013, patients who showed early donor specific anti-HLA antibodies (DSA) after lung tran
25 the biopsy were screened for the presence of donor-specific anti-HLA antibodies (DSAs) and their abil
26 islets and determined that the appearance of donor-specific anti-HLA antibodies (DSAs) did not accele
28 omes in transplant recipients with preformed donor-specific anti-HLA antibodies (pfDSA) managed with
29 and have been postulated to be activated by donor-specific anti-HLA antibodies triggering their CD16
32 t dysfunction and graft loss, development of donor-specific anti-HLA antibodies, and antibody-mediate
33 dividual risk stratification on the basis of donor-specific anti-HLA antibody (anti-HLA DSA) characte
36 2008 and 2010, we enrolled 125 patients with donor-specific anti-human HLA antibodies (DSA) detected
37 ponses in renal transplantation, and de novo donor-specific anti-human leucocyte antigen antibodies (
38 in PB and to analyze their relationship with donor specific antibodies and histological phenotype.
41 is a risk factor for development of de novo donor-specific antibodies (dnDSA) and can contribute to
42 be used in a cohort of patients with de novo donor-specific antibodies (dnDSA) as an early marker to
44 role of protocol kidney biopsies for de novo donor-specific antibodies (dnDSA) in kidney transplant r
49 tients (15.9%) developed anti-VA de novo HLA donor-specific antibodies (dnDSAs) at a median time afte
53 we analyze the impact of low-level preformed donor-specific antibodies (DSA) against an RMM on transp
55 itive cytomegalovirus serostatus (P = 0.02), donor-specific antibodies (DSA) against HLA class II (P
56 T lymphocytes resulted in the generation of donor-specific antibodies (DSA) and AMR, which was assoc
57 ave an increased risk for the development of donor-specific antibodies (DSA) and antibody-mediated re
58 in PB and to analyze their relationship with donor-specific antibodies (DSA) and histological phenoty
59 ibody-mediated rejection (CAABMR), with C4d, donor-specific antibodies (DSA) and other lesions of chr
60 -activating factor (BAFF) is associated with donor-specific antibodies (DSA) and poorer outcomes afte
61 apy selectively depleted mature PC producing donor-specific antibodies (DSA) and reduced DSA, when ad
66 ected at donor human leukocyte antigen (HLA) donor-specific antibodies (DSA) associated with adverse
68 rejection (AMR) driven by the development of donor-specific antibodies (DSA) directed against mismatc
70 and 24 months protocol biopsies and anti-HLA donor-specific antibodies (DSA) in 140 low immunological
71 on into sensitized patients with preexisting donor-specific antibodies (DSA) is very challenging.
73 occur in patients with preexisting anti-HLA donor-specific antibodies (DSA) or in patients who devel
76 is exposed to rapid increases in high-titer donor-specific antibodies (DSA) that are most often gene
77 were: HLA antibodies at transplant, de novo donor-specific antibodies (DSA), antibody-mediated rejec
78 the ability to reduce the incidence of these donor-specific antibodies (DSA), but its mechanism is su
79 ossmatches were achieved against 3, 6, and 8 donor-specific antibodies (DSA), including those that we
86 -DR/DQ molecular mismatch to predict de novo donor-specific antibodies (DSAs) during the first year o
88 -reactive memory T and B cells and preformed donor-specific antibodies (DSAs) have all been implicate
89 y an inhibitory effect on the development of donor-specific antibodies (DSAs) make it an interesting
92 st-transplantation, subjects without de novo donor-specific antibodies (DSAs), AR, or inflammation at
94 %), prior rejection (n=76, 62%), presence of donor-specific antibodies (n=69, 57%), and prior peripar
95 .009), class II anti-human leukocyte antigen donor-specific antibodies (P=0.004), and acute cellular
97 pt exhibited significantly reduced levels of donor-specific antibodies (P=0.05) and bone marrow plasm
98 enal allograft recipients (67 with preformed donor-specific antibodies [DSAs]) with 281 indication bi
99 ansplant inflammation augments generation of donor-specific antibodies against MHC class II antigens.
100 erm graft survival showed gradual rebound of donor-specific antibodies and antibody-mediated rejectio
101 ansplant biopsies from patients with de novo donor-specific antibodies and eighteen 1-year surveillan
104 to 4/18 non-HLA antigens synergize with HLA donor-specific antibodies and significantly increase the
105 ts augment early inflammation in response to donor-specific antibodies and that platelet-derived medi
106 ar, only those who further developed de novo donor-specific antibodies and transplant glomerulopathy
108 azakizumab displayed significantly decreased donor-specific antibodies and, on prolonged treatment, m
114 wed decreased mean fluorescence intensity of donor-specific antibodies as soon as day 12, with no sig
115 s), immunostaining, and circulating anti-HLA donor-specific antibodies at the time of biopsy, togethe
116 the correlative association between IRI and donor-specific antibodies by using humanized models and
118 r-specific HLA antibodies and/or increase in donor-specific antibodies from pretransplant levels are
120 tly reduced anti-HLA antibodies and anti-HLA donor-specific antibodies in a nonhuman primate model an
121 he presence and, importantly, the absence of donor-specific antibodies in an international study of p
122 lation highly expressed IL-18R1 and promoted donor-specific antibodies in response to IL-18 in vivo.
125 croarray allows detailed characterization of donor-specific antibodies necessary for effective transp
129 gnosis of isolated G (isG) in the absence of donor-specific antibodies or G in combination with T cel
132 , and significantly higher levels of class I donor-specific antibodies than those in the Swedish stud
133 rved a significant decrease in class 1 and 2 donor-specific antibodies that led to clinical improveme
136 ter kidney transplant or abrupt increases in donor-specific antibodies when biopsy cannot be performe
137 tion, de novo anti-HLA antibodies (including donor-specific antibodies), and phenotypic differentiati
138 injury (IRI) predisposes to the formation of donor-specific antibodies, a factor contributing to chro
140 ent monitoring for adverse events, outcomes, donor-specific antibodies, and renal function was perfor
141 ironment insults (i.e. abnormal physiology), donor-specific antibodies, and T cell-mediated immunity.
142 MR score was associated with the presence of donor-specific antibodies, biopsy indication, Banff ct,
143 is now clear that VCA recipients can develop donor-specific antibodies, conclusions made in solid org
144 evels of anti-MHC class II (but not class I) donor-specific antibodies, increased donor-reactive T ce
145 macrophage recruitment, suggesting augmented donor-specific antibodies, rather than T cells, increase
146 egies permit transplantation via lowering of donor-specific antibodies, the B cell-response axis from
147 sociated with the risk of developing de novo donor-specific antibodies, therapeutic immunosuppression
157 in the absence of C4d staining or detectable donor-specific antibodies; the potential value of molecu
158 of alloimmune events (development of de novo donor specific antibody and/or biopsy proven rejection)
159 ches serve as potential epitopes for de novo donor specific antibody development and correlate with l
160 = 55 nondirected donors, performance of only donor specific antibody negative transplants, the requir
161 acute rejection episode, malignancy, de novo donor specific antibody, posttransplant diabetes (PTD),
162 ogical and immunohistochemical analysis, and donor- specific antibody (DSA) characterization with the
163 We hypothesized that HLA class II de novo donor-specific antibody (dnDSA) development correlates w
164 me phenotype with the development of de novo donor-specific antibody (DSA) after kidney transplantati
168 ted information exists about outcomes of HLA donor-specific antibody (DSA) negative (DSA-) microvascu
169 e the prevalence and investigate the role of donor-specific antibody (DSA) on intestinal graft outcom
170 lants and pregnancies as sensitizing events, donor-specific antibody (DSA) relative intensity scores
171 sses underlying the induction of deleterious donor-specific antibody (DSA) responses remain poorly un
172 nd treatment of subclinical AMR based on the donor-specific antibody (DSA) testing may result in bett
177 tive traditional FXM results are missing HLA donor-specific antibody 36.2% of the time based on the D
178 FR [eGFR], proteinuria, time posttransplant, donor-specific antibody [DSA]) and molecular and histolo
179 n, old age, no BCG vaccination, and positive donor-specific antibody are also positive predictors for
182 SA-FXM) that distinguishes HLA class I or II donor-specific antibody bound to HLA antigens on the don
185 smatch improved the correlation with de novo donor-specific antibody development (area under the curv
186 mL/min/1.73 m (HR, 2.61; P = 0.011), de novo donor-specific antibody development (HR, 4.09; P < 0.001
187 ted rejection (P = .0006), HLA-DR/DQ de novo donor-specific antibody development (P < .0001), antibod
188 h, variability of tacrolimus trough, de novo donor-specific antibody development, cytochrome P450 3A5
190 in low dd-cfDNA patients (P = .004), de novo donor-specific antibody formation was seen in 40% (17/42
191 xp3(+) cells within donor grafts, diminished donor-specific antibody formation, and delayed rejection
193 immunosuppression for prevention of de novo donor-specific antibody generation at the individual lev
194 ween ongoing inflammation and development of donor-specific antibody has renewed our interest in subc
196 ere the beta2fHC or pepF-beta2aHC normalized donor-specific antibody level would reveal the true anti
197 d with daratumumab had significantly reduced donor-specific antibody levels compared with untreated c
199 organizes germinal center responses, reduces donor-specific antibody levels, and prolongs allograft s
203 t that C1-INH may decrease sensitization and donor-specific antibody production and might improve out
204 , many patients do not respond or experience donor-specific antibody rebound, highlighting the divers
206 ulin (Ig), Qa-1 mutant mice developed robust donor-specific antibody responses and accelerated heart
208 e Banff Working Groups, the relationships of donor-specific antibody tests (anti-HLA and non-HLA) wit
209 n, and 2 cases were presumed on the basis of donor-specific antibody trends and allograft function.
210 histologic features of ABMR were present but donor-specific antibody was undetected (49.4% [43/87]).
212 immunological risk and sensitized (including donor-specific antibody) patients, immunosuppressive com
213 llus Calmette-Guerin (BCG) scar, presence of donor-specific antibody, and KTR group were independent
214 persistently chimeric subject has developed donor-specific antibody, and renal function has remained
215 r in combination with (1/2) dose CsA reduced donor-specific antibody, intragraft transcripts for chem
216 development of human leukocyte antigen (HLA) donor-specific antibody/antibodies (DSA) is not well des
217 significant at 8 years across all levels of donor-specific antibody: 89.2% for recipients of kidney
218 ncluded 20 kidney transplant recipients with donor-specific, antibody-positive ABMR >=365 days post-t
220 aive (untreated) or made immune or tolerant (donor-specific BALB/c splenocyte transfusion -/+ anti-CD
221 llo-hMSC patient developed an elevated (>80) donor-specific calculated panel reactive antibody level.
223 ion, structure, CCL21 presence, and Treg and donor-specific cell location relative to high endothelia
225 pothesized that transplanted tissues release donor-specific exosomes into recipient circulation and t
231 enal allograft recipients with pretransplant donor-specific HLA antibodies (DSA) and its association
232 serum creatinine together with reduction of donor-specific HLA antibodies (DSA) below 500 mean fluor
236 ches (mismatch load) on de novo formation of donor-specific HLA antibodies (DSAs) and transplant outc
237 Post-transplant, development of de novo donor-specific HLA antibodies and/or increase in donor-s
239 nd they were associated with post-transplant donor-specific HLA antibodies, antibody-mediated rejecti
240 bead assays allow for detection of recipient donor-specific HLA antibodies, enabling prediction of co
244 ivity algorithms and the impact of resulting donor-specific HLA antibody (DSA) positivity on long-ter
245 nized that patients may become sensitized to donor-specific HLA antigens as a result of previous anti
246 layed graft function (DGF) and pretransplant donor-specific HLA-antibodies (DSA) are both regarded as
250 ird party antigen, with in vitro evidence of donor-specific hyporesponsiveness in the absence of dono
251 sensitized the recipients as confirmed with donor-specific IgG in the serum, which increased 26-fold
252 accommodation with concurrent inhibition of donor-specific immune memory is likely to be involved.
255 DSCs prolong cardiac allograft survival in a donor-specific manner via induction of recipient's endog
257 is led to the generation of a highly anergic donor-specific medicinal product containing an average o
258 as to investigate the presence of concurrent donor-specific memory B cell-derived HLA antibodies (DSA
260 c allografts were passively transferred with donor-specific MHC I antibodies, mTOR inhibition signifi
262 tional B cell proportions and either de novo donor-specific or nondonor-specific antibody (dnDSA; dnN
263 further stained to define ILC subsets and a donor-specific or recipient-specific HLA marker to analy
264 Hematopoietic chimerism is known to promote donor-specific organ allograft tolerance; however, clini
266 We also analyzed CD8(+) T cell reactivity to donor-specific PBMCs in 24 patients who had received liv
268 short-term LFA-1 blockade promoted long-term donor-specific regulation, which resulted in attenuated
270 Presence/absence of AD-like pathology was donor-specific (reproducible between individual organoid
271 achieve durable hematopoietic chimerism and donor-specific skin allograft tolerance and justify furt
273 th anti-CD40L monoclonal antibody (mAb) plus donor-specific splenocyte transfusion (DST) induces allo
276 anisms through which HCV infection modulates donor-specific T cell responses following LT and the inf
279 ccepted a heart allotransplant and displayed donor-specific tolerance also accepted skin grafts from
280 el nonmyeloablative approach that results in donor-specific tolerance and mixed allogeneic chimerism.
281 rt illustrate that established mechanisms of donor-specific tolerance are strained during potent immu
282 ed lymphocyte reaction and ELISPOT) revealed donor-specific tolerance before and after transplantatio
285 This local immunotherapy imparted systemic donor-specific tolerance in otherwise immunocompetent ra
286 se model of cardiac transplantation in which donor-specific tolerance is induced with costimulation b
287 ionally transplanted patients, thus, whether donor-specific tolerance results in improved outcomes re
293 us abrogating transplantation tolerance, the donor-specific tolerant state re-emerges, allowing spont
294 duced with costimulation blockade (CoB) plus donor-specific transfusion (DST), we have previously sho
295 in stringent animal transplant models using donor-specific transfusions (DST) has previously require
296 c effect in promotion of alloengraftment and donor-specific transplant tolerance, significantly decre
298 romotes the differentiation and expansion of donor-specific Tregs without secondary reprogramming to