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1 al immunity causes little or no damage to an organ graft.
2 resulted in tolerance to the bone marrow and organ grafts.
3 e method for inducing tolerance toward solid organ grafts.
4 ily promote inflammation and injury in solid organ grafts.
5 tion rates remain among the highest of solid organ grafts.
6 rodent models to induce immune tolerance to organ grafts.
7 logic reactions affecting transplanted solid organ grafts.
8 al strategy for prolonging survival of solid organ grafts.
9 mechanisms similar to those affecting solid organ grafts.
10 mechanisms similar to those affecting solid organ grafts.
11 potential to prevent rejection of allogeneic organ grafts.
12 marrow chimerism induces tolerance to solid organ grafts.
13 nduce donor-specific tolerance to xenogeneic organ grafts.
14 ) are often tolerant of donor-specific solid organ grafts.
15 ng specific transplantation tolerance to pig organ grafts.
16 arterial tree of chronically rejecting solid organ grafts.
17 participate in the rejection of interspecies organ grafts.
18 e difficult to manage in recipients of solid organ grafts.
20 nority of cases, continued survival of solid organ grafts after transplantation depends on lifelong,
21 g at increasing the lifespan of vascularized organ grafts also have to take into consideration the re
22 processes, including the rejection of solid organ grafts and graft-versus-host disease (GVHD) follow
25 of life of patients with long-term surviving organ grafts by reducing the immunologic and nonimmunolo
26 to concurrently or subsequently placed solid organ grafts can be reliably achieved with limited numbe
27 The strategy, which is applicable for all organ grafts, constitutes a paradigm shift in transplant
28 was to determine whether tolerance to solid organ grafts could be induced in mice reconstituted with
29 al equal to 1086 recipients of cadaver whole-organ grafts from donors ages 10-40 years who underwent
33 a to normothermia incurred on reperfusion of organ grafts has been delineated as a genuine factor con
36 s variation between donors and recipients of organ grafts in tissue matching, innate immune reactivit
38 s simultaneously infused donor (syngeneic to organ grafts) marrow stem cell engraftment, differentiat
39 consider that what we call accommodation of organ grafts may occur widely in the context of immune r
40 the potential influence of alloantibodies on organ graft outcome, this study investigated the inducti
42 ssive drug therapy-induced impairment of the organ graft recipient's immune surveillance is considere
44 ave reviewed the outcomes for cases of solid organ graft recipients from H1N1 influenza-positive dono
46 ssociated with rejection of allogeneic solid organ grafts, regulatory T (T(reg)) cells appear to fost
48 s needed to overcome the problems of chronic organ graft rejection and immunosuppression-related toxi
49 phingosine 1-phosphate receptors to suppress organ graft rejection in humans and autoimmunity in anim
50 yeloblative total body irradiation prevented organ graft rejection, all hosts succumbed to lethal gra
58 can function as cellular effectors of solid organ graft rejection; however, the specific mechanisms
59 mesenchymal stromal cells can prolong solid organ graft survival and that they can induce immune tol
61 ve association of PRA+ with allogeneic solid organ graft survival has been recognized, but scattered
63 tory events after transplant in solid tissue organ grafts that may direct T cell recruitment and prom
64 are critical for the rejection of some solid organ grafts, the role of CD4(+) T cells in the rejectio
65 c chimerism induces life-long donor-specific organ graft tolerance while obviating the need for chron
66 of early inflammatory events in vascularized organ grafts, we tested the intragraft expression of fou
67 Almost half of all transplanted vascularized organ grafts will be lost to transplant arteriosclerosis
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