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6 ath-censored allograft loss in patients with donor-specific alloantibodies (DSA) mean florescence int
9 idates on waiting lists, and the presence of donor-specific alloantibodies (DSAs) at the time of tran
10 extended allograft survival, indicating that donor-specific alloantibodies (not T cells) were the cri
11 lasmablast numbers, as well as production of donor-specific alloantibodies and complement deposition
12 After perioperative inflammation subsided, donor-specific alloantibodies were passively transferred
16 s at 1-year surveillance biopsy and/or serum donor-specific alloantibody status could improve predict
17 erum creatinine levels, high serum titers of donor-specific alloantibody, minimal T cell infiltration
19 lopment of interstitial fibrosis and de novo donor specific anti-HLA antibodies (dnDSA) at 1 year.
21 until April 2013, patients who showed early donor specific anti-HLA antibodies (DSA) after lung tran
22 epopulating B cells and its correlation with donor-specific anti-HLA Ab development and long-term gra
23 ed with patients with non-complement-binding donor-specific anti-HLA antibodies (93%) and patients wi
24 ti-HLA antibodies (93%) and patients without donor-specific anti-HLA antibodies (94%) (P<0.001 for bo
25 se PTC C4d+ staining had higher frequency of donor-specific anti-HLA antibodies (DSA) (67% and 82%) a
30 the biopsy were screened for the presence of donor-specific anti-HLA antibodies (DSAs) and their abil
31 islets and determined that the appearance of donor-specific anti-HLA antibodies (DSAs) did not accele
34 ere screened for the presence of circulating donor-specific anti-HLA antibodies and their complement-
35 ssment of the complement-binding capacity of donor-specific anti-HLA antibodies appears to be useful
36 al transplant candidates with high levels of donor-specific anti-HLA antibodies have low transplantat
38 and have been postulated to be activated by donor-specific anti-HLA antibodies triggering their CD16
41 dividual risk stratification on the basis of donor-specific anti-HLA antibody (anti-HLA DSA) characte
44 2008 and 2010, we enrolled 125 patients with donor-specific anti-human HLA antibodies (DSA) detected
45 ponses in renal transplantation, and de novo donor-specific anti-human leucocyte antigen antibodies (
47 scribing the incidence and impact of de novo donor-specific anti-human leukocyte antigen (HLA) antibo
48 laries as well as the absence of C1q-binding donor-specific anti-human leukocyte antigen alloantibody
51 d by simultaneous occurrence of pAMR on EMB, donor specific antibodies and allograft dysfunction.
52 converse occurs, and whether changes on non-donor specific antibodies are associated with any outcom
55 s; P<0.001), increased occurrence of de novo donor-specific antibodies (52% vs. 13%; P=0.001), and no
56 is a risk factor for development of de novo donor-specific antibodies (dnDSA) and can contribute to
58 be used in a cohort of patients with de novo donor-specific antibodies (dnDSA) as an early marker to
59 role of protocol kidney biopsies for de novo donor-specific antibodies (dnDSA) in kidney transplant r
62 In renal transplant patients with de novo donor-specific antibodies (dnDSA) we studied the value o
65 itive cytomegalovirus serostatus (P = 0.02), donor-specific antibodies (DSA) against HLA class II (P
66 g Banff 2007 criteria along with presence of donor-specific antibodies (DSA) and acute rise in serum
67 ibody-mediated rejection (CAABMR), with C4d, donor-specific antibodies (DSA) and other lesions of chr
71 ected at donor human leukocyte antigen (HLA) donor-specific antibodies (DSA) associated with adverse
75 and 24 months protocol biopsies and anti-HLA donor-specific antibodies (DSA) in 140 low immunological
76 on into sensitized patients with preexisting donor-specific antibodies (DSA) is very challenging.
78 occur in patients with preexisting anti-HLA donor-specific antibodies (DSA) or in patients who devel
80 were: HLA antibodies at transplant, de novo donor-specific antibodies (DSA), antibody-mediated rejec
81 verity of each patient and were negative for donor-specific antibodies (DSA), C4d, and microcirculati
86 antibodies are the predominant HLA class II donor-specific antibodies (DSAs) after transplantation.
92 y an inhibitory effect on the development of donor-specific antibodies (DSAs) make it an interesting
93 phocyte/flow crossmatch was negative; and if donor-specific antibodies (DSAs) were absent in the firs
95 st-transplantation, subjects without de novo donor-specific antibodies (DSAs), AR, or inflammation at
97 enal allograft recipients (67 with preformed donor-specific antibodies [DSAs]) with 281 indication bi
100 ansplant biopsies from patients with de novo donor-specific antibodies and eighteen 1-year surveillan
102 ts augment early inflammation in response to donor-specific antibodies and that platelet-derived medi
103 cases because of the presence of high titer donor-specific antibodies and the potential of the liver
104 ar, only those who further developed de novo donor-specific antibodies and transplant glomerulopathy
108 wed decreased mean fluorescence intensity of donor-specific antibodies as soon as day 12, with no sig
109 s), immunostaining, and circulating anti-HLA donor-specific antibodies at the time of biopsy, togethe
110 ugh none of the nine subjects had detectable donor-specific antibodies before or after transplantatio
114 with an increased risk of developing de novo donor-specific antibodies during the first year posttran
115 r-specific HLA antibodies and/or increase in donor-specific antibodies from pretransplant levels are
116 he presence and, importantly, the absence of donor-specific antibodies in an international study of p
119 croarray allows detailed characterization of donor-specific antibodies necessary for effective transp
122 gnosis of isolated G (isG) in the absence of donor-specific antibodies or G in combination with T cel
125 , and significantly higher levels of class I donor-specific antibodies than those in the Swedish stud
126 participate in allograft lesions mediated by donor-specific antibodies through antibody-dependent cel
128 o the donor or immunity masked by binding of donor-specific antibodies to the graft is not known.
129 llaritis (g>/=1 and ptc>/=1) with detectable donor-specific antibodies was observed in some recipient
130 llaritis (g>/=1 and ptc>/=1) with detectable donor-specific antibodies was observed in some recipient
133 merulitis and detectable posttransplantation donor-specific antibodies were risk factors for TxGN (P<
134 merulitis and detectable posttransplantation donor-specific antibodies were risk factors for TxGN (P<
135 m anti-HLA antibodies to donor HLA antigens (donor-specific antibodies) and serum MHC class 1-related
136 ients (negative flow crossmatch and positive donor-specific antibodies) treated with tacrolimus.
137 ury, (2) may occur before the development of donor-specific antibodies, (3) predict the development o
138 toring revealed transient moderate levels of donor-specific antibodies, adequate immunocompetence, an
139 eloped anti-HLA antibodies, of which 6% were donor-specific antibodies, and 6% developed anti-MICA an
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,
144 tches, and/or the presence of high levels of donor-specific antibodies, on the outcomes of simultaneo
145 sociated with the risk of developing de novo donor-specific antibodies, therapeutic immunosuppression
156 ches serve as potential epitopes for de novo donor specific antibody development and correlate with l
157 = 55 nondirected donors, performance of only donor specific antibody negative transplants, the requir
158 fined as 3 of 4 criteria: renal dysfunction, donor specific antibody, C4d positivity on biopsy, and h
159 We hypothesized that HLA class II de novo donor-specific antibody (dnDSA) development correlates w
163 e the prevalence and investigate the role of donor-specific antibody (DSA) on intestinal graft outcom
164 lants and pregnancies as sensitizing events, donor-specific antibody (DSA) relative intensity scores
165 1 for cause biopsies [FCBx]) with concurrent donor-specific antibody (DSA) studies, C4d staining, and
166 ly associated with the generation of de novo donor-specific antibody (DSA), antibody-mediated-rejecti
170 aft outcomes among patients desensitized for donor-specific antibody (HLA-incompatible) is unknown.
171 ) after adjustment for pretransplant/de novo donor-specific antibody and delayed graft function.
174 xp3(+) cells within donor grafts, diminished donor-specific antibody formation, and delayed rejection
177 creatinine, panel reactive antibody levels, donor-specific antibody frequency, or mean fluorescence
178 immunosuppression for prevention of de novo donor-specific antibody generation at the individual lev
180 nel-reactive antibody was 60+/-33 and median donor-specific antibody level was a mean fluorescence in
181 ere the beta2fHC or pepF-beta2aHC normalized donor-specific antibody level would reveal the true anti
184 living donors/151 deceased donors) patients (donor-specific antibody positive, PRA>80%) were desensit
187 es a prognostic value independent of initial donor-specific antibody status, previous immunologic eve
189 e Banff Working Groups, the relationships of donor-specific antibody tests (anti-HLA and non-HLA) wit
190 population was 267 consecutive patients with donor-specific antibody undergoing desensitization.
192 immunological risk and sensitized (including donor-specific antibody) patients, immunosuppressive com
193 sing serum creatinine with marked rebound of donor-specific antibody, and a biopsy that showed featur
194 sensitized recipients (positive cross-match, donor-specific antibody, and elevated panel reactive ant
195 persistently chimeric subject has developed donor-specific antibody, and renal function has remained
196 r in combination with (1/2) dose CsA reduced donor-specific antibody, intragraft transcripts for chem
198 all exhibited increases in the frequency of donor-specific antibody-secreting cells eight weeks afte
201 CI], 1.37 to 3.58; P=0.001) and endothelial donor-specific antibody-selective transcripts (HR, 3.02;
205 significant at 8 years across all levels of donor-specific antibody: 89.2% for recipients of kidney
206 A2(+) skin allografts resulted in a surge of donor-specific (antiYHLA.A2) immunoglobulin (Ig)G antibo
207 troversial, however, is the possibility that donor-specific B cells and the Abs that they produce are
211 aive (untreated) or made immune or tolerant (donor-specific BALB/c splenocyte transfusion -/+ anti-CD
212 llo-hMSC patient developed an elevated (>80) donor-specific calculated panel reactive antibody level.
214 6B to cross-present donor antigens to induce donor-specific CD8(+) CD11c(+) T cells with regulatory p
215 ion, structure, CCL21 presence, and Treg and donor-specific cell location relative to high endothelia
218 pothesized that transplanted tissues release donor-specific exosomes into recipient circulation and t
219 f CD8 T cells from HIV(+) and HIV(neg) human donors, specific for HIV and/or respiratory syncytial vi
221 ificant DSA antibody rise no significant non-donor specific HLA antibody, viral or blood group antibo
222 antibodies, of which 52 (36.9%) were de novo donor-specific HLA antibodies (DSA) (34 SPK, 18 IP).
224 serum creatinine together with reduction of donor-specific HLA antibodies (DSA) below 500 mean fluor
228 d analysis of patient and graft survival and donor-specific HLA antibodies (DSA) were performed.
230 Post-transplant, development of de novo donor-specific HLA antibodies and/or increase in donor-s
234 nd they were associated with post-transplant donor-specific HLA antibodies, antibody-mediated rejecti
235 bead assays allow for detection of recipient donor-specific HLA antibodies, enabling prediction of co
238 nized that patients may become sensitized to donor-specific HLA antigens as a result of previous anti
241 pients mounted responses to CMV presented by donor-specific HLA, despite the detection of CMV antigen
243 im was to determine the incidence of de novo donor-specific human leukocyte antigen (HLA) antibody (d
248 accommodation with concurrent inhibition of donor-specific immune memory is likely to be involved.
249 of mixed hematopoietic chimerism results in donor-specific immunological tolerance by apoptosis-medi
254 is led to the generation of a highly anergic donor-specific medicinal product containing an average o
256 c allografts were passively transferred with donor-specific MHC I antibodies, mTOR inhibition signifi
259 tional B cell proportions and either de novo donor-specific or nondonor-specific antibody (dnDSA; dnN
260 further stained to define ILC subsets and a donor-specific or recipient-specific HLA marker to analy
261 Hematopoietic chimerism is known to promote donor-specific organ allograft tolerance; however, clini
263 rial follow-up of peripheral blood indicated donor-specific posttransplant unresponsiveness in micro-
266 short-term LFA-1 blockade promoted long-term donor-specific regulation, which resulted in attenuated
268 achieve durable hematopoietic chimerism and donor-specific skin allograft tolerance and justify furt
270 th anti-CD40L monoclonal antibody (mAb) plus donor-specific splenocyte transfusion (DST) induces allo
272 over the long term; they exhibited increased donor-specific suppressive functions; and their removal
274 We next performed allogeneic IUHCTx into donor-specific T-cell receptor transgenic mice and confi
277 ccepted a heart allotransplant and displayed donor-specific tolerance also accepted skin grafts from
278 el nonmyeloablative approach that results in donor-specific tolerance and mixed allogeneic chimerism.
279 rt illustrate that established mechanisms of donor-specific tolerance are strained during potent immu
280 ed lymphocyte reaction and ELISPOT) revealed donor-specific tolerance before and after transplantatio
281 ion (IUHCTx) is a promising method to induce donor-specific tolerance but the mechanisms of antigen p
282 le for up to 2 years and was associated with donor-specific tolerance for renal transplantation.
284 amycin and IL-2/Fc fusion protein results in donor-specific tolerance to VCA, but not FTS allografts.
285 w) subpopulation, which are able to transfer donor-specific tolerance via IL-10 and TGF-beta1-depende
287 oal in transplantation is the achievement of donor-specific tolerance, minimizing the use of immunosu
291 us abrogating transplantation tolerance, the donor-specific tolerant state re-emerges, allowing spont
292 we aimed at testing the ability to generate donor-specific Tr1 cell-enriched lymphocytes from patien
293 le of stem cell transplantation (SCT) versus donor-specific transfusion (DST) in tolerance induction
294 ine heart transplant recipients treated with donor-specific transfusion (DST) plus anti-CD154 monoclo
296 c effect in promotion of alloengraftment and donor-specific transplant tolerance, significantly decre
297 romotes the differentiation and expansion of donor-specific Tregs without secondary reprogramming to
299 develop an adoptive therapy with tolerogenic donor-specific type 1 T regulatory cells for patients wi
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