ライフサイエンスコーパス: veto cell

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

2 capable of protein synthesis to function as veto cells.

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

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

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

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

7 CD8 veto cells are an antigen-specific immunoregulatory cell

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

28 6 tetramer(+) CTL cocultured with AKR.H-2(b) veto cells was annexin V positive and Fas(high), indicat

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

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

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