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1 s immune response in the clinical setting of acute graft rejection.
2 h a subnormal renal function and early-stage acute graft rejection.
3 tment is necessary for the efferent phase of acute graft rejection.
4 on has been limited by the high incidence of acute graft rejection.
5 t recipients correlates with the presence of acute graft rejection.
6 s in both the priming and effector phases of acute graft rejection.
7 human cardiac allograft specimens undergoing acute graft rejection.
8 ity in the transplanted hearts indicative of acute graft rejection.
9 hin host lymphoid tissue, is associated with acute graft rejection.
10 r antibodies nor CD8+ T cells participate in acute graft rejection.
11 for two decades to reverse steroid-resistant acute graft rejection.
12 ents in this study, irrespective of interval acute graft rejection.
13 R3 is a viable therapeutic target to prevent acute graft rejection.
14 CD4+ T cells are the primary mediators of acute graft rejection, although complement may contribut
15 reased recipient age, African American race, acute graft rejection and CMV infection were significant
16 sociated with the pharmacologic avoidance of acute graft rejection and the development of chronic tis
17 s strategy and could be used both to prevent acute graft rejection as well as for maintenance immunos
18 cells are both necessary and sufficient for acute graft rejection, as indicated by adoptive transfer
19 h cyclosporine, markedly attenuated not only acute graft rejection but also alloantibody elaboration
20 sk for posttransplant mortality, graft loss, acute graft rejection, chronic rejection, cancer, infect
23 ells correlates closely with the presence of acute graft rejection in renal allograft recipients.
24 ogeneic blood transfusion causes accelerated acute graft rejection in the presence of the complete co
25 At six months, the rate of biopsy-confirmed acute graft rejection in the seronegative group was 52 p
27 F) has been shown to reduce the incidence of acute graft rejection in three controlled trials of cada
28 normally observed and resulted in delayed or acute graft rejection (median survival times, 40 and 12
30 t recipients to account for the avoidance of acute graft rejection or the development of chronic tiss
31 : 18.76; 95% CI: 1.04-339.37; p = 0.047) and acute graft rejection (OR: 40.73, 95% CI: 3.63-456.98; p
32 ential to revise the clinical perspective on acute graft rejection, pending the results of larger stu
33 esponse is likely to be the driving force in acute graft rejection, posttransplantation induced autoi
34 ion of P5-activated syngeneic T cells led to acute graft rejection, suggesting that the homing of in
35 though it is believed that Th1 cells promote acute graft rejection, the role of these cells in chroni
36 e may expedite the noninvasive prediction of acute graft rejection, thus importantly assisting in est
37 To further investigate the role of LTs in acute graft rejection, we transplanted kidneys from CByD
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