ライフサイエンスコーパス: acute allograft rejection

1 OR (LysM(C)(re) Mtor(fl/fl) ) did not affect acute allograft rejection.

2 tion to the response to steroid treatment of acute allograft rejection.

3 cance of common specific vascular lesions in acute allograft rejection.

4 vein endothelitis, which is consistent with acute allograft rejection.

5 ty and indicate instead that it is a form of acute allograft rejection.

6 rate levels, may serve as an early marker of acute allograft rejection.

7 nt targets in some liver diseases, including acute allograft rejection.

8 is that donor-reactive TH1 cells can promote acute allograft rejection.

9 ssumed that IFNgamma plays a central role in acute allograft rejection.

10 orecognition pathway participate actively in acute allograft rejection.

11 3 inhibitors R507 and R545 for prevention of acute allograft rejection.

12 ed with AKI and 9 (4.9%) were diagnosed with acute allograft rejection.

13 serve as early serum markers for monitoring acute allograft rejection.

14 sponses during an infection, malignancy, and acute allograft rejection.

15 by donor DCs is alone insufficient to elicit acute allograft rejection.

16 al models does not play an essential role in acute allograft rejection.

17 tion, nor alters Th1 immune responses during acute allograft rejection.

18 at shock protein (HSP)-70 is associated with acute allograft rejection.

19 JAK3 inhibition with CP-690,550 prevents acute allograft rejection.

20 activation of specific leukocyte subsets in acute allograft rejection.

21 with or without immunosuppression to prevent acute allograft rejection.

22 e independently predicts a decreased risk of acute allograft rejection.

23 ents, of whom 23 (64%) showed some degree of acute allograft rejection.

24 dent and IFN-gamma-independent mechanisms of acute allograft rejection.

25 appaB activation in T cells is necessary for acute allograft rejection.

26 imary targets of host CTL-mediated injury in acute allograft rejection.

27 cytotoxic during cardiac, hepatic, and renal acute allograft rejection.

28 showed profound resistance to development of acute allograft rejection.

29 would be a major advance in the treatment of acute allograft rejection.

30 transplantation model was used for studying acute allograft rejection.

31 are now used routinely for the diagnosis of acute allograft rejection.

32 osuppressive agent used for the treatment of acute allograft rejection.

33 these cells into SCID recipients resulted in acute allograft rejection.

34 of IL-2, IL-4, IL-7, and IL-15 genes during acute allograft rejection.

35 selectively deplete monocyte/macrophages in acute allograft rejection, although this did not result

36 level of CD40L transcripts is evident during acute allograft rejection and (ii) the kinetics of CD40L

37 ts were excluded from analysis (5 because of acute allograft rejection and 4 because of poor acoustic

38 Gs) are used clinically to prevent and treat acute allograft rejection and are believed to modulate t

39 17 has recently been observed in settings of acute allograft rejection and drives rejection in T-bet-

40 VEGF may play a role in the pathogenesis of acute allograft rejection and it may serve as a reliable

41 merican patients demonstrate higher rates of acute allograft rejection and lower kidney-graft surviva

42 s considered important in the development of acute allograft rejection and many other immune-mediated

43 ve therapy in response to specific grades of acute allograft rejection and may result in decreased co

44 The anti-CD154 antibody hu5C8 prevents acute allograft rejection and prolongs allograft surviva

45 that HSP-70 levels are not increased during acute allograft rejection and that an absence of the ind

46 how that TLRs are involved in the process of acute allograft rejection and that their activation can

47 sterol, low density lipoprotein cholesterol, acute allograft rejection and time since transplantation

48 of immune activation is controversial during acute allograft rejection and unknown in xenotransplanta

49 alitatively similar to those observed during acute allograft rejection, and (3) no specific immune re

50 oth costimulatory blockade, which suppresses acute allograft rejection, and a favorable balance betwe

51 rt correlates directly with the evolution of acute allograft rejection, and that immunosuppressive th

52 se herbal preparation, CMX-13, on inhibiting acute allograft rejection (AR) in a highly histoincompat

53 ted renal allograft nephropathy (BKVAN) from acute allograft rejection (AR) in renal transplant recip

54 reported, patients experience high rates of acute allograft rejection (AR).

55 ed transplant patients it is associated with acute allograft rejection as well as chronic allograft v

56 cidence of biopsy proven grade II or greater acute allograft rejection at 6 months was 58% in the AZA

57 ejection, but rather caused a delayed severe acute allograft rejection at approximately 45 days postt

58 lineage have been implicated as effectors in acute allograft rejection based on short-term depletion

59 Pichinde virus also induced acute allograft rejection, but murine cytomegalovirus an

60 receptors [TCR]) are known to be crucial for acute allograft rejection, but the role of other members

61 /macrophages are recognized as a hallmark of acute allograft rejection, but the roles that they play

62 ctivation pathway with CS1 peptides prevents acute allograft rejection by inhibiting expansion of ant

63 Currently, acute allograft rejection can only be detected reliably

64 To determine if acute allograft rejection could induce these proteins in

65 ade, delayed OX40 stimulation did not induce acute allograft rejection despite priming of graft-react

66 onal immunosuppressive strategies that check acute allograft rejection do not prevent TV; indeed 50%

67 The primary endpoint of the study was acute allograft rejection during a 1-year follow-up peri

68 f sirolimus reduced the overall incidence of acute allograft rejection episodes to 7.5% from 32% in t

69 ed clinical or histopathological evidence of acute allograft rejection episodes, cytokine release syn

70 to immunosuppressive regimens, treatment of acute allograft rejection, feeding, and viral surveillan

71 respective cut-off, accurately discriminates acute allograft rejection from other causes of AKI in fo

72 diagnosis of AKI, accurately discriminating acute allograft rejection from other causes of AKI in re

73 e of the indirect allorecognition pathway in acute allograft rejection has been documented both in or

74 Acute allograft rejection has often been correlated with

75 orrelations between bacterial infections and acute allograft rejection have been reported.

76 Human and animal studies of acute allograft rejection have implicated CCR5 and CXCR3

77 the inducible form of HSP-70 neither delays acute allograft rejection, impairs DCs maturation, nor a

78 0 activates DCs and plays a critical role in acute allograft rejection in an experimental model that

79 udy, we examine the participation of TLR4 in acute allograft rejection in an orthotopic mouse model o

80 molecules has been efficacious in preventing acute allograft rejection in certain but not all transpl

81 ex vivo-expanded natural Treg could prevent acute allograft rejection in mice.

82 between elevated cardiac troponin levels and acute allograft rejection in patients who have received

83 It effectively prevented acute allograft rejection in several experimental transp

84 cells can play an obligate role for primary acute allograft rejection in vivo.

85 ical observations showing significantly less acute allograft rejections in recipients having high IgM

86 Acute allograft rejection is a major complication of lun

87 Acute allograft rejection is a major complication postlu

88 Acute allograft rejection is considered to be a predomin

89 The hallmark of acute allograft rejection is infiltration of the inflame

90 ection and induces tolerance in experimental acute allograft rejection models.

91 kidney transplantation, we demonstrated that acute allograft rejection occurred equally in MyD88-suff

92 iopsies obtained from individuals undergoing acute allograft rejection of various solid organs.

93 fragments and the presence of biopsy-proven acute allograft rejection or AGA (assessed by coronary a

94 , and according to underlying pathology into acute allograft rejection or AKI of other cause.

95 e observed that (1) IL-4 is not required for acute allograft rejection or allogeneic DTH responses in

96 The primary study endpoint was biopsy-proven acute allograft rejection over the first 6 months posttr

97 as ligand (FasL), is closely correlated with acute allograft rejection, particularly when two or more

98 perforin expression correlates strongly with acute allograft rejection, perforin-deficient mice rejec

99 cells had arrived at the graft-but promoted acute allograft rejection rather than allograft acceptan

100 substances that activate these cells during acute allograft rejection remain elusive.

101 at may direct T cell recruitment and promote acute allograft rejection remain largely unknown.

102 Acute allograft rejection remains an important cause of

103 Acute allograft rejection requires a multifaceted immune

104 Acute allograft rejection requires the activation of all

105 ys posttransplantation for assessment of the acute allograft rejection response.

106 graft leukocyte infiltration and in reducing acute allograft rejection scores.

107 TLA4-Ig and 5C8 can both prevent and reverse acute allograft rejection, significantly prolonging the

108 ransplant and restored the histopathology of acute allograft rejection to that observed in allografts

109 In acute allograft rejection, urinary NGAL concentration wa

110 study, we investigated the role of IL-17 in acute allograft rejection using IL-17-deficient mice.

111 Thus, VEGF appears to be functional in acute allograft rejection via its effects on leukocyte t

112 Acute allograft rejection was characterized by a varying

113 Acute allograft rejection was diagnosed by endomyocardia

114 ls in vivo, their role in the progression of acute allograft rejection was unclear.

115 of T cell-intrinsic NF-kappaB activation in acute allograft rejection, we used IkappaBalphaDeltaN-Tg

116 ipients experiencing biopsy-proven recurrent acute allograft rejection were eligible if the current r

117 determine whether MMF decreases episodes of acute allograft rejection when compared with azathioprin

118 rchetypical cell-mediated immune response of acute allograft rejection, whereas TH2 cells promote all

119 h1 response has been shown to play a role in acute allograft rejection, whereas the Th2 response has

120 23, p = 0.0014), as well as the diagnosis of acute allograft rejection, which is preceded by increase

121 (C5b-C9) has been demonstrated previously in acute allograft rejection with the use of C6-deficient P

122 ce bearing B6 cardiac allografts resulted in acute allograft rejection within 5 to 10 days.

123 aring B6 cardiac allografts also resulted in acute allograft rejection within 7 to 10 days.