ライフサイエンスコーパス: veto

1 Our data suggest that subjects can still veto a movement even after the onset of the RP.

2 CD8+ allo-BMC are enriched for veto activity and activation via CD8 induces TGF-beta1 m

3 expresses more TGF-beta1 mRNA and increased veto activity at low BMC/CTLp ratios.

4 CD8+ cells were tested for veto activity by mixed lymphocyte reaction (MLR)-induced

5 rrow in parental recipients, suggesting that veto activity is not restricted solely to the CD8 subset

6 Veto activity was measured by both visualizing apoptosis

7 over-express active TGF-beta1 might mediate veto activity without the need to express CD8alpha.

8 a1 mRNA after CD8 cross-linking, and exhibit veto activity.

9 c) inhibitory input is exquisitely suited to veto an NMDA spike if it arrives within a 30 ms window i

10 The use of clinician veto and adjudication is discouraged.

11 ing the unintended consequences of clinician veto and clinical adjudication panels.

12 his large subpopulation are neurons known to veto and regulate the synchrony of principal cell spikin

13 These L chains diminish or veto anti-DNA binding when expressed with anti-DNA H cha

14 th "editor" L chains that did not completely veto autoreactivity.

15 cantly extended the window of opportunity to veto based deletion by preventing the responding 2C T ce

16 , responding T cells are only susceptible to veto based deletion for a 48-hour window, which represen

17 ing rapamycin, the window of opportunity for veto-based induction of tolerance to transplantation ant

18 essant drugs were tested for their effect on veto cell activity.

19 ssed the effect of inflammatory mediators on veto cell activity.

20 ted, contact dependent, and mediated through veto cell Fas ligand/responder T cell Fas interactions.

21 AKR.H-2(b) veto cell inhibition is virus specific, MHC restricted,

22 h), indicating apoptosis as the mechanism of veto cell inhibition.

23 These findings may help to explain why veto cell-based therapies are more effective than other

24 etected after subsequent immunization with a veto cell-expressed Ag.

25 Conceptually, veto cell-expressed antigens (Ags) may induce B-cell imm

26 Of the tetramer-positive CTL that survived veto cell-mediated apoptosis, there was no marked skewin

27 enabling direct visualization of AKR.H-2(b) veto cell-mediated depletion of these CTL.

28 is in T cells that recognize antigens on the veto cell.

29 CD8 veto cells are an antigen-specific immunoregulatory cell

30 Accordingly, the authors hypothesized that veto cells are resistant to the effects of innate immune

31 Lacking TCRs, these veto cells are unlikely to mediate graft-versus-host dis

32 represents a severe limitation to the use of veto cells as a cellular therapeutic.

33 nts a serious obstacle in the development of veto cells as an efficacious cellular therapy to induce

34 lock inhibition demonstrated that AKR.H-2(b) veto cells begin to inhibit B6 precursor CTL/CTL expansi

35 BALB/c veto cells exhibited a potent and antigen-specific delet

36 Whether veto cells induce immunity, tolerance, or are ignored by

37 The authors demonstrate that the activity of veto cells is unaltered by lipopolysaccharide, double-st

38 stimulation cultures of either 1) AKR.H-2(b) veto cells or 2) a blocking Fas-Ig fusion protein (to cu

39 Unlike other strategies, veto cells promote long-term allograft survival in prima

40 6 tetramer(+) CTL cocultured with AKR.H-2(b) veto cells was annexin V positive and Fas(high), indicat

41 CD8 veto cells were generated from BALB/c (H-2) mice.

42 tly inhibited the veto effect, but only when veto cells were limiting.

43 tein (to cultures also containing AKR.H-2(b) veto cells) to block inhibition demonstrated that AKR.H-

44 capable of protein synthesis to function as veto cells.

45 CD8(alpha)alpha lymphoid dendritic cells and veto cells.

46 ecursors to antigens expressed by those CD8+ veto cells.

47 ursor CTL, the AKR.H-2(b) cells function as "veto" cells that actively mediate the inhibition of anti

48 In vivo, the administration of veto CTL also induced B-cell tolerance.

49 Veto CTL are effective promoters of B-cell tolerance.

50 y-specific cytotoxic T lymphocytes (CTL), or veto CTL, are being assessed as a cellular therapeutic f

51 ced with a model cell surface Ag to generate veto CTL.

52 t Ag-specific B cells were eliminated by the veto CTL; the cell division was accompanied by the exhau

53 in normal livers, in fibrosis, LSECs do not veto dendritic cell priming of T cells.

54 egulatory changes, but Notch/Delta signaling vetoes diversion.

55 Here, we studied whether the veto effect could be exploited for this purpose neverthe

56 The so-called veto effect has been described as one such technology wh

57 necrosis factor-alpha modestly inhibited the veto effect, but only when veto cells were limiting.

58 eactive T cells and has been attributed to a veto effect.

59 nal transduction within the BMCs to increase veto effector molecules such as transforming growth fact

60 s the use of clinical adjudication panels to veto events that meet HAI surveillance definitions.The H

61 ordingly, nonattractive features effectively veto female responses.

62 T cell proliferation, it does not affect the veto function of IFN-gamma MSCs on both T cell prolifera

63 ecipher the mechanistic underpinnings of MSC veto function on T cells, we investigated the effect of

64 immune-enhancing properties, MSCs also exert veto functions and show evidence for allogeneic transpla

65 Veto-induced B-cell tolerance could be wholly abrogated

66 HAb specifically and effectively transferred veto inhibition to different stimulator cell populations

67 Yet, veto inhibition will not be able to provide complete tol

68 ropose that the interneurons that supply the vetoing inhibition define these modular circuit territor

69 nt here data indicating a pivotal role for a vetoing inhibition restraining modules of pyramidal neur

70 a graft-vs-host reaction, they also exerted veto-like activity, but caused no effect on responses to

71 all Ags, we examined whether MSC could exert veto-like functions.

72 A veto mechanism could enable donor T cells to prevent all

73 olerogenic effect of allo-BMC, ascribed to a veto mechanism, associates with specific functional dele

74 against donor class I alloantigens through a veto mechanism, whereas the absence of MHC class II mole

75 he area, because of a feedforward inhibitory veto mechanism.

76 e precursor enhances their susceptibility to veto-mediated functional inactivation by specific alloan

77 ctivity into a desynchronized mode simply by vetoing occasional RE cell bursts.

78 can act synergistically to provide a global veto of dendritic excitability.

79 s shift is not obligatory but that it may be vetoed on the basis of expectation.

80 identified, that recipient has the "right of veto" on the research, (4) patients should be able to pa

81 This IFN-gamma-licensed veto property is IDO-dependent.

82 necessarily giving communities the power to veto research proposals; and (4) the conflation of socia

83 P + 1 position in substrates functions as a "veto" residue in substrate recognition by AGC and CAMK k

84 e cells originate in the thymus and potently veto responses to Dd in vitro.

85 censed dendritic cells, on the one hand, and veto suppression by live male lymphocytes on the other.

86 which CTLA-4 control of immunity goes beyond vetoing T-cell priming and encompasses the regulation of

87 However, whether CTLA-4 acts simply to veto the activation of certain clones or plays a more nu

88 from 2-3 AACs on average, were necessary to veto the PC firing under our recording conditions.

89 ediated signal to phagocytic host cells that vetoes the bacterial evasion strategies, thereby efficie

90 ), exerts a spatially offset inhibition that vetoes the response of DSGCs to image movement in a spec

91 favor of and against allowing relatives to "veto" the potential donor's intentions.

92 expressing FasL inhibit antiviral T cells ("veto" them) when the AKR.H-2(b) cells are recognized.