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1 T cells, is important for the maintenance of allograft tolerance.
2 insight into selective gene suppression and allograft tolerance.
3 induce memory T cell exhaustion can promote allograft tolerance.
4 (mAb) treatment is very potent in producing allograft tolerance.
5 is not necessarily associated with specific allograft tolerance.
6 as well as the induction of transplantation allograft tolerance.
7 ens for the induction of mixed chimerism and allograft tolerance.
8 of donor T cells and B cells in BMC-induced allograft tolerance.
9 lls that are essential in the maintenance of allograft tolerance.
10 m to be essential for the promotion of liver allograft tolerance.
11 ndent mechanism governing the acquisition of allograft tolerance.
12 llograft tolerance, a very stringent test of allograft tolerance.
13 controls, are resistant to the induction of allograft tolerance.
14 poptosis, as well as the induction of stable allograft tolerance.
15 e grafted liver may be responsible for liver allograft tolerance.
16 cells may be critical in the acquisition of allograft tolerance.
17 ransplantation may provide a means to induce allograft tolerance.
18 nt implications for therapeutic induction of allograft tolerance.
19 loantigens in adult mice, it might result in allograft tolerance.
20 mechanisms for induction and maintenance of allograft tolerance.
21 icant effect, induced donor specific cardiac allograft tolerance.
22 cal role in the induction and maintenance of allograft tolerance.
23 ting a regulatory role in the maintenance of allograft tolerance.
24 immunoregulatory phenotypes and may promote allograft tolerance.
25 suggest an approach to achieving intestinal allograft tolerance.
26 increased durable donor-specific BALB/c skin allograft tolerance.
27 have shown that TMEM176B is associated with allograft tolerance.
28 ene 88 (MyD88) induced donor-specific kidney allograft tolerance.
29 vity in the lymph node during peripheral and allograft tolerance.
30 chimerism leads to long-term donor-specific allograft tolerance.
31 pressed in ATDCs and initially identified in allograft tolerance.
32 in the nevertheless long-term persistence of allograft tolerance.
33 ) regulatory T cells (Tregs) to induce islet allograft tolerance.
34 but little is known regarding their roles in allograft tolerance.
35 kine, IL-4, and specific alloantigen promote allograft tolerance.
36 ne responses whilst simultaneously promoting allograft tolerance.
37 een studied in several models including skin allograft tolerance.
38 erging B cell directed strategies to achieve allograft tolerance.
39 d Th2 responses, and could directly transfer allograft tolerance.
40 donor macrophages as a new target to achieve allograft tolerance.
41 (-/-) mice prevented autoimmunity and led to allograft tolerance.
42 idonor T-effector cell responses and promote allograft tolerance.
43 ect against infectious disease or to promote allograft tolerance.
44 face interaction, therefore inducing cardiac allograft tolerance.
45 ling allograft rejection or perhaps inducing allograft tolerance.
46 ly anecdotal, clinical experience with organ allograft tolerance.
47 islet allograft survival and donor-specific allograft tolerance.
48 loantigen-specific Treg cell development and allograft tolerance.
49 etion of CD25(+) T cells in vivo broke islet allograft tolerance.
50 e critical for the acquisition of peripheral allograft tolerance.
51 regulatory cells are not critical for islet allograft tolerance.
52 resistant to costimulation blockade-induced allograft tolerance.
53 raftment is considered to be an indicator of allograft tolerance.
54 e same HA-1 antigen, in the context of renal allograft tolerance.
55 o-stimulatory signals would facilitate islet allograft tolerance.
56 Histology suggested functional allograft tolerance.
58 lloreactive T cells and produced stable skin allograft tolerance, a very stringent test of allograft
59 has been considered to be a prerequisite for allograft tolerance after bone marrow transplantation (B
60 ) promoted hematopoietic chimerism and renal allograft tolerance after partial deletion of HSCs and e
61 basis for the resistance of NOD mice to skin allograft tolerance also applies to islet allografts.
62 ically applicable approach to inducing renal allograft tolerance and achieving potent and sustained a
63 lass II could have important implications in allograft tolerance and in developing class II-deficient
64 necessary and sufficient for inducing islet allograft tolerance and is necessary but not sufficient
65 atopoietic chimerism and donor-specific skin allograft tolerance and justify further development of a
67 rating full reconstitution and donor cardiac-allograft tolerance and no GVHD with expanded donor and
70 erm follow-up data show that sustained renal allograft tolerance and prolonged antimyeloma responses
72 created in this way generates donor-specific allograft tolerance and reverses the predisposition to r
74 L) treatment to induce robust donor-specific allograft tolerance and suppress the alloantibody respon
76 to manipulate Treg cell activity to promote allograft tolerance and treat autoimmunity, chronic infe
77 d in latent infection-mediated resistance to allograft tolerance and underscore the influence of late
78 netic loss of CoREST in Tregs impaired organ allograft tolerance and unleashed antitumor immunity via
79 ckpoints play an important role in self- and allograft-tolerance and risk of acute allograft rejectio
80 hat: 1) Fas is not necessarily essential for allograft tolerance, and 2) Fas-mediated apoptosis is no
81 s in clinical protocols for the induction of allograft tolerance, and for the application of such pro
82 ucidate mechanisms of antitumor immunity and allograft tolerance, and inform updates to transplant de
83 therapy improved donor engraftment, promoted allograft tolerance, and prevented graft-versus-host dis
84 rtantly, a monoclonal anti-TIM-4 Ab promoted allograft tolerance, and this was dependent on B cell ex
86 ell engraftment is required for induction of allograft tolerance, but not for creation of continuous
87 chimerism are not required for induction of allograft tolerance by the antilymphocyte serum/rapamyci
88 dy, we demonstrate that a stable MC and skin allograft tolerance can be established across MHC barrie
90 data suggest that the induction of dominant allograft tolerance dependent on regulatory T cells does
91 omotion of hematopoietic chimerism and renal allograft tolerance despite using only half of the dose
92 demonstrate a setting in which the memory of allograft tolerance dominates over the memory of transpl
94 th tacrolimus plus ortho IL-2 achieved heart allograft tolerance, even after tacrolimus cessation, wh
97 ism is known to promote donor-specific organ allograft tolerance; however, clinical translation has b
98 s identify IL-34 as an important mediator of allograft tolerance in a rat model of heart transplantat
100 ides CD8(+) Tregs, could induce and maintain allograft tolerance in CD40Ig-treated tolerant animals.
101 a simple, safe, and effective way to induce allograft tolerance in clinical organ transplantation.
106 MHC class I-dependent NK cell reactivity for allograft tolerance in mice induced through either costi
107 es durable mixed hematopoietic chimerism and allograft tolerance in mice receiving allogeneic bone ma
110 Anti-CD3-immunotoxin (alpha-CD3-IT) promotes allograft tolerance in nonhuman primates owing to effici
111 perforin competent are sufficient to restore allograft tolerance in perforin-deficient recipients.
113 Perioperative lymphocyte depletion induces allograft tolerance in some animal models, but in humans
114 Interestingly, MR1 anti-CD154 induces islet allograft tolerance in the absence of CD40/CD154 pathway
116 and mechanism of action of Tregs in inducing allograft tolerance in transplantation, are still not fu
119 ously demonstrated in a rat model of cardiac allograft tolerance induced by short-term immunosuppress
120 e encephalomyelitis, Tph-1 deficiency breaks allograft tolerance, induces tumor remission, and intens
121 n of MHC class II Ag on BMC is essential for allograft tolerance induction and peripheral chimerism w
127 ta demonstrate that 1) NOD mice resist islet allograft tolerance induction; 2) unlike skin allografts
128 gene(s) is an important determinant of islet allograft tolerance induction; and 4) there may be overl
130 unlike skin allografts, resistance to islet allograft tolerance is a genetically recessive trait; 3)
131 roviding proof of principle that operational allograft tolerance is attainable in clinical transplant
135 induction of T-cell apoptosis and peripheral allograft tolerance is prevented by blocking both signal
136 One of the biggest barriers to achieving allograft tolerance is the presence of immunological mem
139 uous immunosuppression, a condition known as allograft tolerance, is a highly desirable therapeutic g
140 1 as overexpressed in a model of rat cardiac allograft tolerance mediated by regulatory CD4CD25 T cel
142 iruses that establish a true latent state on allograft tolerance or the effect of tolerance protocols
144 cription factor (Tbet) KO recipients exhibit allograft tolerance resistance specifically mediated by
145 e have used this T17-biased Tbet KO model of allograft tolerance resistance to study the impact of ta
146 for the induction and maintenance of kidney allograft tolerance since renal allotransplantation into
149 ved antigen-specific tolerance in a model of allograft tolerance through CD154 blockade are presented
150 e during the induction and/or maintenance of allograft tolerance through creation of MC using a poten
151 In the current study, we attempted to induce allograft tolerance through the mixed chimerism approach
152 We also show that mast cells are crucial for allograft tolerance, through the inability to induce tol
154 mixed chimerism is required for murine skin allograft tolerance (TOL), renal allograft TOL has been
158 alloreactive BCR, we recently reported that allograft tolerance was associated with the sustained de
160 llografts experienced prolonged engraftment; allograft tolerance was frequently achieved in the DBA/2
162 th clinical and phenotypic parameters, renal allograft tolerance was strongly associated with a B cel
163 of costimulation blockade-dependent cardiac allograft tolerance, we previously reported that allorea
164 tive at ICAM-1 blockade, and induced cardiac allograft tolerance when combined with LFA-1 monoclonal
165 erestingly, disruption of coronin 1 promotes allograft tolerance while immunity towards a range of pa
166 e purpose of the present study was to induce allograft tolerance with a protocol compatible with dece
167 sential initial step for induction of stable allograft tolerance with non-lymphoablative therapy.
168 initial step in the induction of peripheral allograft tolerance with regimens that are not inherentl
169 ovide proof-of-concept for establishing lung allograft tolerance with tandem donor bone marrow transp
170 4 blockade induced mixed chimerism and renal allograft tolerance, with significantly less morbidity a
171 ntinuing need for agents capable of inducing allograft tolerance without generalized immunosuppressio
172 c chimerism resulted in donor specific renal allograft tolerance without the need for chronic immunos