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1 ated rejection on the basis of histology and donor-specific antibody.
2 the presence of microcirculation lesions and donor-specific antibody.
3 , and occur more frequently in patients with donor-specific antibody.
4 s, peritubular capillary C4d deposition, and donor-specific antibodies.
5 rejection, viral infections, and class 1 HLA donor-specific antibodies.
6 mediated rejection (ABMR) in the presence of donor-specific antibodies.
7 ble, and 22 recipients had unacceptably high donor-specific antibodies.
8 and allograft dysfunction in recipients with donor-specific antibodies.
9 mechanisms underlying the downregulation of donor-specific antibodies.
10 e 1-year eGFR only in kidney recipients with donor-specific antibodies.
11 zation and the development of posttransplant donor-specific antibodies.
12 or suboptimal immunosuppression and de novo donor-specific antibodies.
13 ate into germinal center B cells and secrete donor-specific antibodies.
14 ntation in infants, who cease producing only donor-specific antibodies.
15 ates, C4d positivity and high serum anti-HLA donor-specific antibodies.
16 osition and significant decline in their HLA donor-specific antibodies.
17 ated rejection confirmed by demonstration of donor-specific antibodies.
18 h protocol biopsy and development of de novo donor-specific antibodies.
19 nd tubular atrophy), as well as with de novo donor-specific antibodies.
20 levels of anti-class 2 but not anti-class 1 donor-specific antibodies.
22 ury, (2) may occur before the development of donor-specific antibodies, (3) predict the development o
23 tive traditional FXM results are missing HLA donor-specific antibody 36.2% of the time based on the D
24 s; P<0.001), increased occurrence of de novo donor-specific antibodies (52% vs. 13%; P=0.001), and no
25 significant at 8 years across all levels of donor-specific antibody: 89.2% for recipients of kidney
26 injury (IRI) predisposes to the formation of donor-specific antibodies, a factor contributing to chro
28 ivariate survival predictors were absence of donor-specific antibody, absence of recipient splenectom
30 toring revealed transient moderate levels of donor-specific antibodies, adequate immunocompetence, an
31 er pretransplant panel reactive antibody and donor-specific antibody affected KTx outcome in SLK.
34 ansplant inflammation augments generation of donor-specific antibodies against MHC class II antigens.
35 d by simultaneous occurrence of pAMR on EMB, donor specific antibodies and allograft dysfunction.
36 in PB and to analyze their relationship with donor specific antibodies and histological phenotype.
37 of alloimmune events (development of de novo donor specific antibody and/or biopsy proven rejection)
39 erm graft survival showed gradual rebound of donor-specific antibodies and antibody-mediated rejectio
40 ansplant biopsies from patients with de novo donor-specific antibodies and eighteen 1-year surveillan
43 to 4/18 non-HLA antigens synergize with HLA donor-specific antibodies and significantly increase the
44 ts augment early inflammation in response to donor-specific antibodies and that platelet-derived medi
45 cases because of the presence of high titer donor-specific antibodies and the potential of the liver
46 ar, only those who further developed de novo donor-specific antibodies and transplant glomerulopathy
48 azakizumab displayed significantly decreased donor-specific antibodies and, on prolonged treatment, m
50 m anti-HLA antibodies to donor HLA antigens (donor-specific antibodies) and serum MHC class 1-related
51 tion, de novo anti-HLA antibodies (including donor-specific antibodies), and phenotypic differentiati
52 eloped anti-HLA antibodies, of which 6% were donor-specific antibodies, and 6% developed anti-MICA an
53 ent monitoring for adverse events, outcomes, donor-specific antibodies, and renal function was perfor
54 ironment insults (i.e. abnormal physiology), donor-specific antibodies, and T cell-mediated immunity.
55 sing serum creatinine with marked rebound of donor-specific antibody, and a biopsy that showed featur
56 sensitized recipients (positive cross-match, donor-specific antibody, and elevated panel reactive ant
57 llus Calmette-Guerin (BCG) scar, presence of donor-specific antibody, and KTR group were independent
58 persistently chimeric subject has developed donor-specific antibody, and renal function has remained
59 development of human leukocyte antigen (HLA) donor-specific antibody/antibodies (DSA) is not well des
60 converse occurs, and whether changes on non-donor specific antibodies are associated with any outcom
65 C4d deposits in the skin and circulating donor-specific antibodies are rarely detected, suggestin
67 n, old age, no BCG vaccination, and positive donor-specific antibody are also positive predictors for
68 wed decreased mean fluorescence intensity of donor-specific antibodies as soon as day 12, with no sig
69 s), immunostaining, and circulating anti-HLA donor-specific antibodies at the time of biopsy, togethe
72 ugh none of the nine subjects had detectable donor-specific antibodies before or after transplantatio
74 MR score was associated with the presence of donor-specific antibodies, biopsy indication, Banff ct,
75 SA-FXM) that distinguishes HLA class I or II donor-specific antibody bound to HLA antigens on the don
76 the correlative association between IRI and donor-specific antibodies by using humanized models and
78 fined as 3 of 4 criteria: renal dysfunction, donor specific antibody, C4d positivity on biopsy, and h
80 is now clear that VCA recipients can develop donor-specific antibodies, conclusions made in solid org
82 With Luminex single antigen bead technology, donor-specific antibodies could be identified before ris
84 ious transplants, panel reactive antibodies, donor specific antibody, crossmatches (CMXs), patient an
87 ches serve as potential epitopes for de novo donor specific antibody development and correlate with l
88 smatch improved the correlation with de novo donor-specific antibody development (area under the curv
89 mL/min/1.73 m (HR, 2.61; P = 0.011), de novo donor-specific antibody development (HR, 4.09; P < 0.001
90 ted rejection (P = .0006), HLA-DR/DQ de novo donor-specific antibody development (P < .0001), antibod
91 h, variability of tacrolimus trough, de novo donor-specific antibody development, cytochrome P450 3A5
92 is a risk factor for development of de novo donor-specific antibodies (dnDSA) and can contribute to
94 be used in a cohort of patients with de novo donor-specific antibodies (dnDSA) as an early marker to
96 role of protocol kidney biopsies for de novo donor-specific antibodies (dnDSA) in kidney transplant r
99 In renal transplant patients with de novo donor-specific antibodies (dnDSA) we studied the value o
102 We hypothesized that HLA class II de novo donor-specific antibody (dnDSA) development correlates w
103 tients (15.9%) developed anti-VA de novo HLA donor-specific antibodies (dnDSAs) at a median time afte
106 of chronic rejection (CR) is multifactorial, donor specific antibody (DSA) is considered to have a ca
107 afts can be elicited by adoptive transfer of donor specific antibody (DSA) to class I MHC antigens an
108 ogical and immunohistochemical analysis, and donor- specific antibody (DSA) characterization with the
111 we analyze the impact of low-level preformed donor-specific antibodies (DSA) against an RMM on transp
113 itive cytomegalovirus serostatus (P = 0.02), donor-specific antibodies (DSA) against HLA class II (P
114 g Banff 2007 criteria along with presence of donor-specific antibodies (DSA) and acute rise in serum
115 T lymphocytes resulted in the generation of donor-specific antibodies (DSA) and AMR, which was assoc
117 ave an increased risk for the development of donor-specific antibodies (DSA) and antibody-mediated re
118 in PB and to analyze their relationship with donor-specific antibodies (DSA) and histological phenoty
119 ibody-mediated rejection (CAABMR), with C4d, donor-specific antibodies (DSA) and other lesions of chr
120 -activating factor (BAFF) is associated with donor-specific antibodies (DSA) and poorer outcomes afte
122 apy selectively depleted mature PC producing donor-specific antibodies (DSA) and reduced DSA, when ad
128 ected at donor human leukocyte antigen (HLA) donor-specific antibodies (DSA) associated with adverse
130 e role of anti-human leukocyte antigen (HLA) donor-specific antibodies (DSA) detected by Luminex in t
132 rejection (AMR) driven by the development of donor-specific antibodies (DSA) directed against mismatc
135 and 24 months protocol biopsies and anti-HLA donor-specific antibodies (DSA) in 140 low immunological
136 on into sensitized patients with preexisting donor-specific antibodies (DSA) is very challenging.
138 occur in patients with preexisting anti-HLA donor-specific antibodies (DSA) or in patients who devel
141 er C1q-fixing antibodies distinguish de novo donor-specific antibodies (DSA) that are clinically rele
142 is exposed to rapid increases in high-titer donor-specific antibodies (DSA) that are most often gene
143 AND Of 37 AMR+ patients, 22 (60%) developed donor-specific antibodies (DSA) to HLA compared with 6 o
144 or every 2 months, a test was performed for donor-specific antibodies (DSA) using Luminex mixed and/
145 were: HLA antibodies at transplant, de novo donor-specific antibodies (DSA), antibody-mediated rejec
146 the ability to reduce the incidence of these donor-specific antibodies (DSA), but its mechanism is su
147 verity of each patient and were negative for donor-specific antibodies (DSA), C4d, and microcirculati
148 ossmatches were achieved against 3, 6, and 8 donor-specific antibodies (DSA), including those that we
149 nd correlated with morphology, ELISA screen, donor-specific antibodies (DSA), response to treatment,
156 me phenotype with the development of de novo donor-specific antibody (DSA) after kidney transplantati
157 idney-combined organ recipients with de novo donor-specific antibody (DSA) and histologic evidence of
164 ceived renal transplants with a pretreatment donor-specific antibody (DSA) level of more than 500 in
165 We have demonstrated that immunodominant donor-specific antibody (DSA) more than 100 mean fluores
166 ted information exists about outcomes of HLA donor-specific antibody (DSA) negative (DSA-) microvascu
167 e the prevalence and investigate the role of donor-specific antibody (DSA) on intestinal graft outcom
168 lants and pregnancies as sensitizing events, donor-specific antibody (DSA) relative intensity scores
169 sses underlying the induction of deleterious donor-specific antibody (DSA) responses remain poorly un
170 1 for cause biopsies [FCBx]) with concurrent donor-specific antibody (DSA) studies, C4d staining, and
171 nd treatment of subclinical AMR based on the donor-specific antibody (DSA) testing may result in bett
172 of this study were to determine the level of donor-specific antibody (DSA) that allows for successful
173 based on the results of a VXM, in which the donor-specific antibody (DSA) was prospectively evaluate
175 ly associated with the generation of de novo donor-specific antibody (DSA), antibody-mediated-rejecti
180 FR [eGFR], proteinuria, time posttransplant, donor-specific antibody [DSA]) and molecular and histolo
182 human leukocyte antigen (HLA) antibodies and donor-specific antibodies (DSAs) after early graft loss
184 antibodies are the predominant HLA class II donor-specific antibodies (DSAs) after transplantation.
189 -DR/DQ molecular mismatch to predict de novo donor-specific antibodies (DSAs) during the first year o
190 re excluded from matching to recipients with donor-specific antibodies (DSAs) greater than 2000 mean
192 -reactive memory T and B cells and preformed donor-specific antibodies (DSAs) have all been implicate
195 y an inhibitory effect on the development of donor-specific antibodies (DSAs) make it an interesting
197 phocyte/flow crossmatch was negative; and if donor-specific antibodies (DSAs) were absent in the firs
200 st-transplantation, subjects without de novo donor-specific antibodies (DSAs), AR, or inflammation at
201 f therapies targeting removal of circulating donor-specific antibodies (DSAs), blocking their effect
203 enal allograft recipients (67 with preformed donor-specific antibodies [DSAs]) with 281 indication bi
204 with an increased risk of developing de novo donor-specific antibodies during the first year posttran
206 in low dd-cfDNA patients (P = .004), de novo donor-specific antibody formation was seen in 40% (17/42
207 xp3(+) cells within donor grafts, diminished donor-specific antibody formation, and delayed rejection
211 creatinine, panel reactive antibody levels, donor-specific antibody frequency, or mean fluorescence
212 r-specific HLA antibodies and/or increase in donor-specific antibodies from pretransplant levels are
213 immunosuppression for prevention of de novo donor-specific antibody generation at the individual lev
215 ween ongoing inflammation and development of donor-specific antibody has renewed our interest in subc
216 aft outcomes among patients desensitized for donor-specific antibody (HLA-incompatible) is unknown.
218 zed patients with positive FC crossmatch and donor-specific antibody identified by solid phase assays
221 tly reduced anti-HLA antibodies and anti-HLA donor-specific antibodies in a nonhuman primate model an
222 he presence and, importantly, the absence of donor-specific antibodies in an international study of p
223 lation highly expressed IL-18R1 and promoted donor-specific antibodies in response to IL-18 in vivo.
228 evels of anti-MHC class II (but not class I) donor-specific antibodies, increased donor-reactive T ce
229 r in combination with (1/2) dose CsA reduced donor-specific antibody, intragraft transcripts for chem
231 nel-reactive antibody was 60+/-33 and median donor-specific antibody level was a mean fluorescence in
232 ere the beta2fHC or pepF-beta2aHC normalized donor-specific antibody level would reveal the true anti
233 d with daratumumab had significantly reduced donor-specific antibody levels compared with untreated c
235 organizes germinal center responses, reduces donor-specific antibody levels, and prolongs allograft s
238 lack of immunological surveillance-including donor-specific antibody monitoring, human leukocyte anti
239 %), prior rejection (n=76, 62%), presence of donor-specific antibodies (n=69, 57%), and prior peripar
240 croarray allows detailed characterization of donor-specific antibodies necessary for effective transp
241 = 55 nondirected donors, performance of only donor specific antibody negative transplants, the requir
242 reactive antibody less than 20%, absence of donor-specific antibody, negative crossmatch, warm ische
247 tches, and/or the presence of high levels of donor-specific antibodies, on the outcomes of simultaneo
248 gnosis of isolated G (isG) in the absence of donor-specific antibodies or G in combination with T cel
250 h the donor as well as the pretransplant HLA-donor specific antibodies (P=0.002) were associated with
251 .009), class II anti-human leukocyte antigen donor-specific antibodies (P=0.004), and acute cellular
253 pt exhibited significantly reduced levels of donor-specific antibodies (P=0.05) and bone marrow plasm
254 immunological risk and sensitized (including donor-specific antibody) patients, immunosuppressive com
256 living donors/151 deceased donors) patients (donor-specific antibody positive, PRA>80%) were desensit
257 -fixed paraffin-embedded tissues (FFPE) from donor-specific antibody-positive (DSA+) renal allograft
258 ncluded 20 kidney transplant recipients with donor-specific, antibody-positive ABMR >=365 days post-t
259 acute rejection episode, malignancy, de novo donor specific antibody, posttransplant diabetes (PTD),
260 The clinical significance of pretransplant donor-specific antibodies (pre-Tx DSAs) detected by sing
261 t that C1-INH may decrease sensitization and donor-specific antibody production and might improve out
262 macrophage recruitment, suggesting augmented donor-specific antibodies, rather than T cells, increase
263 , many patients do not respond or experience donor-specific antibody rebound, highlighting the divers
266 te was associated with (1) abrogation of the donor-specific antibody response, (2) transient preponde
267 ulin (Ig), Qa-1 mutant mice developed robust donor-specific antibody responses and accelerated heart
270 all exhibited increases in the frequency of donor-specific antibody-secreting cells eight weeks afte
273 CI], 1.37 to 3.58; P=0.001) and endothelial donor-specific antibody-selective transcripts (HR, 3.02;
277 es a prognostic value independent of initial donor-specific antibody status, previous immunologic eve
279 e Banff Working Groups, the relationships of donor-specific antibody tests (anti-HLA and non-HLA) wit
280 , and significantly higher levels of class I donor-specific antibodies than those in the Swedish stud
281 rved a significant decrease in class 1 and 2 donor-specific antibodies that led to clinical improveme
282 egies permit transplantation via lowering of donor-specific antibodies, the B cell-response axis from
283 in the absence of C4d staining or detectable donor-specific antibodies; the potential value of molecu
284 sociated with the risk of developing de novo donor-specific antibodies, therapeutic immunosuppression
285 participate in allograft lesions mediated by donor-specific antibodies through antibody-dependent cel
288 o the donor or immunity masked by binding of donor-specific antibodies to the graft is not known.
289 ients (negative flow crossmatch and positive donor-specific antibodies) treated with tacrolimus.
290 n, and 2 cases were presumed on the basis of donor-specific antibody trends and allograft function.
291 population was 267 consecutive patients with donor-specific antibody undergoing desensitization.
293 llaritis (g>/=1 and ptc>/=1) with detectable donor-specific antibodies was observed in some recipient
294 histologic features of ABMR were present but donor-specific antibody was undetected (49.4% [43/87]).
298 merulitis and detectable posttransplantation donor-specific antibodies were risk factors for TxGN (P<
299 dent cytotoxicity assay, of 77+/-19% or with donor-specific antibodies) were enrolled and received tr
300 ter kidney transplant or abrupt increases in donor-specific antibodies when biopsy cannot be performe