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1            It is incompletely understood how donor-specific Ab binding to graft endothelium promotes
2                 Importantly, the subclass of donor-specific Ab may influence its pathogenesis.
3                     Gp2 became sensitized to donor-specific AB-I or pig antigens within 2 weeks.
4 x-detected anti-HLA Abs classes I and II and donor-specific Abs (DSA) classes I and II.
5     Sensitized recipients with pretransplant donor-specific Abs are at higher risk for Ab-mediated re
6 ath-censored allograft loss in patients with donor-specific alloantibodies (DSA) mean florescence int
7 ntigen, zinc transporter type 8 antigen) and donor-specific alloantibodies (DSA) were quantified.
8 LT) recipients with preformed or de novo HLA donor-specific alloantibodies (DSA).
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
13                       No recipients produced donor-specific alloantibodies.
14                       Adding the presence of donor-specific alloantibody at 1 year did not improve pr
15 n of host sensitization based on circulating donor-specific alloantibody levels.
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
18  Enhanced mixed chimerism leads to long-term donor-specific allograft tolerance.
19 lopment of interstitial fibrosis and de novo donor specific anti-HLA antibodies (dnDSA) at 1 year.
20                                      De novo donor specific anti-HLA antibodies (dnDSA) may cause gra
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
26                                              Donor-specific anti-HLA antibodies (DSA) are a major cau
27                                Screening for donor-specific anti-HLA antibodies (DSA) using bead-base
28 acteristics (allograft biopsy specimen), and donor-specific anti-HLA antibodies (DSA).
29 y indicate the clinical relevance of de novo donor-specific anti-HLA antibodies (DSA).
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
32           The presence of complement-binding donor-specific anti-HLA antibodies after transplantation
33             Patients with complement-binding donor-specific anti-HLA antibodies after transplantation
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
37                    Adding complement-binding donor-specific anti-HLA antibodies to a traditional risk
38  and have been postulated to be activated by donor-specific anti-HLA antibodies triggering their CD16
39                                  Circulating donor-specific anti-HLA antibodies were significantly as
40                                  Circulating donor-specific anti-HLA antibodies were significantly as
41 dividual risk stratification on the basis of donor-specific anti-HLA antibody (anti-HLA DSA) characte
42                            With standard IgG donor-specific anti-HLA antibody (DSA) testing, it is un
43 ons (55% vs 11%, P < 0.01) with detection of donor-specific anti-HLAabs.
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 (
46      Patients with pretransplantation strong donor-specific anti-human leukocyte antigen (HLA) antibo
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
49                Many patients develop de novo donor-specific anti-human leukocyte antigen antibodies (
50                           Although preformed donor-specific anti-human leukocyte antigen antibodies (
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
53                                         C1q+ donor specific antibodies were reduced in 2 C1-INH treat
54 %) and their recipient had unacceptably high donor-specific antibodies (28%).
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
57        Recent evidence suggests that de novo donor-specific antibodies (dnDSA) are associated with an
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
60                        Production of de novo donor-specific antibodies (dnDSA) is a major risk factor
61                       Development of de novo donor-specific antibodies (dnDSA) is associated with lat
62    In renal transplant patients with de novo donor-specific antibodies (dnDSA) we studied the value o
63                                      De novo donor-specific antibodies (dnDSAs) have been associated
64                               Development of donor-specific antibodies (DSA) after lung transplantati
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
68                                   High titer donor-specific antibodies (DSA) and positive crossmatch
69               It is widely accepted that HLA donor-specific antibodies (DSA) are associated with anti
70                                              Donor-specific antibodies (DSA) are considered as reliab
71 ected at donor human leukocyte antigen (HLA) donor-specific antibodies (DSA) associated with adverse
72                                  Circulating donor-specific antibodies (DSA) cause profound changes i
73                                  Circulating donor-specific antibodies (DSA) detected on bead arrays
74                        Postkidney transplant donor-specific antibodies (DSA) have been identified as
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.
77                      Presence of circulating donor-specific antibodies (DSA) may be associated with w
78  occur in patients with preexisting anti-HLA donor-specific antibodies (DSA) or in patients who devel
79           Anti-HLA antibodies and especially donor-specific antibodies (DSA) play a significant role
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
82 ive (CM) patients were tested for C1q-fixing donor-specific antibodies (DSA).
83 study including 85 biopsies of patients with donor-specific antibodies (DSA).
84 radigm with respect to the interpretation of donor-specific antibodies (DSA).
85 , such as capillary C4d or complement-fixing donor-specific antibodies (DSA).
86  antibodies are the predominant HLA class II donor-specific antibodies (DSAs) after transplantation.
87               Complement-activating anti-HLA donor-specific antibodies (DSAs) are associated with imp
88                                 Preexisting, donor-specific antibodies (DSAs) are culprits of hyperac
89                  The effect of low titers of donor-specific antibodies (DSAs) detected only by sensit
90                                  The role of donor-specific antibodies (DSAs) in AAD, with the increa
91  but the relationship between BK viremia and donor-specific antibodies (DSAs) is unexplored.
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
94  (IgG) subclass and C1q binding activity for donor-specific antibodies (DSAs) were determined.
95 st-transplantation, subjects without de novo donor-specific antibodies (DSAs), AR, or inflammation at
96 ith the presence of TRIs (P=0.04) along with donor-specific antibodies (P=0.01).
97 enal allograft recipients (67 with preformed donor-specific antibodies [DSAs]) with 281 indication bi
98                      Although a link between donor-specific antibodies against human leukocyte antige
99                                  Preexisting donor-specific antibodies against human leukocyte antige
100 ansplant biopsies from patients with de novo donor-specific antibodies and eighteen 1-year surveillan
101                   IdeS reduced or eliminated donor-specific antibodies and permitted HLA-incompatible
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
105           Eighty-six of these recipients had donor-specific antibodies and underwent protocol biopsy,
106                                              Donor-specific antibodies are also formed de novo, and t
107                  Current therapies to modify donor-specific antibodies are limited and ineffective in
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
111                                              Donor-specific antibodies create an immunologic barrier
112                                              Donor-specific antibodies detected by solid-phase assays
113                                              Donor-specific antibodies detected by solid-phase assays
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
117 itivity for human leukocyte antigen class II donor-specific antibodies in the R group.
118 totoxicity against stromal cells coated with donor-specific antibodies in vitro.
119 croarray allows detailed characterization of donor-specific antibodies necessary for effective transp
120                                      Neither donor-specific antibodies nor vascular Cd4 deposits were
121                       The negative effect of donor-specific antibodies on the success of solid transp
122 gnosis of isolated G (isG) in the absence of donor-specific antibodies or G in combination with T cel
123                                 The existing donor-specific antibodies or moderate microvascular infl
124                       Whether the absence of donor-specific antibodies reflects absence of a B cell r
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
127                             AMR is caused by donor-specific antibodies to HLA, which contribute to TA
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
131                                              Donor-specific antibodies were elevated in three patient
132                                              Donor-specific antibodies were evaluated using solid-pha
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,
143                The four diagnostic tenets of donor-specific antibodies, C4d staining, histopathologic
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
146 mediated rejection (ABMR) in the presence of donor-specific antibodies.
147 ble, and 22 recipients had unacceptably high donor-specific antibodies.
148 and allograft dysfunction in recipients with donor-specific antibodies.
149  mechanisms underlying the downregulation of donor-specific antibodies.
150 e 1-year eGFR only in kidney recipients with donor-specific antibodies.
151 zation and the development of posttransplant donor-specific antibodies.
152  or suboptimal immunosuppression and de novo donor-specific antibodies.
153 s, peritubular capillary C4d deposition, and donor-specific antibodies.
154 rejection, viral infections, and class 1 HLA donor-specific antibodies.
155                 The second patient developed donor-specific antibodies; some months after CT were fir
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
160                 We hypothesized that de novo donor-specific antibody (DSA) causes complement-dependen
161         On average, the level of HLA class I donor-specific antibody (DSA) decreased by 32%, whereas
162                                     Avoiding donor-specific antibody (DSA) is difficult for sensitize
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
167 R decline by halting the progression of late donor-specific antibody (DSA)-positive ABMR.
168 part by increasing circulation/production of donor-specific antibody (DSA).
169 idual donor-recipient HLA mismatch to induce donor-specific antibody (DSA).
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.
172                                              Donor-specific antibody avoidance and reduction strategi
173 al transplant patients who had no detectable donor-specific antibody before transplantation.
174 xp3(+) cells within donor grafts, diminished donor-specific antibody formation, and delayed rejection
175 ral clearance while preventing rejection and donor-specific antibody formation.
176                                 Overall mean donor-specific antibody frequencies were comparable for
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
179                   Because the development of donor-specific antibody is associated with early graft l
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
182                                              Donor-specific antibody levels were measured by single a
183 ntation grade (P<0.001) and association with donor-specific antibody levels.
184 living donors/151 deceased donors) patients (donor-specific antibody positive, PRA>80%) were desensit
185                                   Those with donor-specific antibody requiring desensitization and in
186                            The strength of a donor-specific antibody should be assessed with a bead-s
187 es a prognostic value independent of initial donor-specific antibody status, previous immunologic eve
188                                              Donor-specific antibody strength and number were reduced
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.
191                      De novo alloantibodies (donor-specific antibody) contribute to antibody-mediated
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
197                 The increase in frequency of donor-specific antibody-secreting cells after renal tran
198  all exhibited increases in the frequency of donor-specific antibody-secreting cells eight weeks afte
199                                We enumerated donor-specific antibody-secreting cells in the blood of
200 ts: the ABMR Molecular Score and endothelial donor-specific antibody-selective transcript set.
201  CI], 1.37 to 3.58; P=0.001) and endothelial donor-specific antibody-selective transcripts (HR, 3.02;
202 ated rejection on the basis of histology and donor-specific antibody.
203 the presence of microcirculation lesions and donor-specific antibody.
204 , and occur more frequently in patients with donor-specific antibody.
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
208           Scarcely anyone would dispute that donor-specific B cells and the Abs that they produce can
209        Using novel tracking tools to monitor donor-specific B cells, alloreactive B cells were shown
210 , clodronate pre-treatment increased durable donor-specific BALB/c skin allograft tolerance.
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.
213                                   Endogenous donor-specific CD8 T cells were tracked down using major
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
216  recipients of male donors for chromosome Y (donor)-specific dd-cfDNA.
217       Hence, this method is suitable for the donor specific enrichment and proteomic analysis of neur
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
220 specific expression show that iPSCs retain a donor-specific gene expression pattern.
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).
223                                  The role of donor-specific HLA antibodies (DSA) after pediatric live
224  serum creatinine together with reduction of donor-specific HLA antibodies (DSA) below 500 mean fluor
225                          The role of de novo donor-specific HLA antibodies (DSA) in liver transplanta
226                       Complement fixation by donor-specific HLA antibodies (DSA) is a primary mechani
227                           The development of donor-specific HLA antibodies (DSA) is associated with w
228 d analysis of patient and graft survival and donor-specific HLA antibodies (DSA) were performed.
229                           The association of donor-specific HLA antibodies (DSA) with kidney graft fa
230      Post-transplant, development of de novo donor-specific HLA antibodies and/or increase in donor-s
231                                              Donor-specific HLA antibodies increased in two patients
232                                              Donor-specific HLA antibodies significantly lower allogr
233 e identified in two additional patients (non-donor-specific HLA antibodies).
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
236 ntibody-mediated rejection in the absence of donor-specific HLA antibodies.
237  on histology (microcirculation lesions) and donor-specific HLA antibody.
238 nized that patients may become sensitized to donor-specific HLA antigens as a result of previous anti
239                  These findings suggest that donor-specific HLA class I antibodies directly activate
240                                              Donor-specific HLA sensitization developed in 2 MPC and
241 pients mounted responses to CMV presented by donor-specific HLA, despite the detection of CMV antigen
242                                      De novo donor-specific human leukocyte antigen (HLA) antibodies
243 im was to determine the incidence of de novo donor-specific human leukocyte antigen (HLA) antibody (d
244                           The development of donor-specific human leukocyte antigen (HLA) class I ant
245 is a more robust biomarker of tolerance than donor-specific hyporeactivity.
246                             All demonstrated donor-specific hyporesponsiveness and were weaned from f
247 linical rejection on protocol biopsy despite donor-specific hyporesponsiveness.
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
250                                              Donor-specific immunological tolerance using high doses
251                                              Donor-specific induced pluripotent stem cells (iPSC) can
252 ion primary response gene 88 (MyD88) induced donor-specific kidney allograft tolerance.
253 hich these cells prolong graft survival in a donor-specific manner is unknown.
254 is led to the generation of a highly anergic donor-specific medicinal product containing an average o
255                   In the experimental model, donor-specific MHC I antibodies significantly increased
256 c allografts were passively transferred with donor-specific MHC I antibodies, mTOR inhibition signifi
257 c allografts were passively transferred with donor-specific MHC I antibodies.
258                 We report the observation of donor-specific mitochondrial cfDNA in the circulation of
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
262 ositive antibodies, although not necessarily donor-specific (P < 0.001).
263 rial follow-up of peripheral blood indicated donor-specific posttransplant unresponsiveness in micro-
264            AR were associated with increased donor-specific production of interferon (IFN)-gamma and
265 within host retinae that express an array of donor-specific proteins.
266 short-term LFA-1 blockade promoted long-term donor-specific regulation, which resulted in attenuated
267                    We previously showed that donor-specific regulatory T-lymphocytes prevent rejectio
268  achieve durable hematopoietic chimerism and donor-specific skin allograft tolerance and justify furt
269           Tolerance was not observed because donor-specific skin graft rechallenge in nonrejecting an
270 th anti-CD40L monoclonal antibody (mAb) plus donor-specific splenocyte transfusion (DST) induces allo
271                                       BALB/c donor-specific splenocyte transfusion and anti-CD40L mon
272 over the long term; they exhibited increased donor-specific suppressive functions; and their removal
273                                              Donor-specific T-cell migration was visualized by adopti
274     We next performed allogeneic IUHCTx into donor-specific T-cell receptor transgenic mice and confi
275          We observed progressive deletion of donor-specific T-lymphocytes, accounting at least in par
276 us to achieve mixed allogeneic chimerism and donor-specific tolerance (DST).
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.
283                 These data demonstrated that donor-specific tolerance to all components of the VCA ca
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
286                                              Donor-specific tolerance was assessed with mixed lymphoc
287 oal in transplantation is the achievement of donor-specific tolerance, minimizing the use of immunosu
288 emonstrated to effectively induce allogeneic donor-specific tolerance.
289 thout immunosuppression to assess for robust donor-specific tolerance.
290 stem cell transplantation (HSCT) can lead to donor-specific tolerance.
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
295 gan transplant, a clinical method defined as donor-specific transfusion (DST).
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
298 etion of effector cells without expansion of donor-specific Tregs.
299 develop an adoptive therapy with tolerogenic donor-specific type 1 T regulatory cells for patients wi
300                           The results showed donor-specific variations in dose dependent deformabilit

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