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1 LAK cell efficacy for three patients with EBV- PTLD was
2 LAK cells are also capable of Fas ligand-mediated cytoto
3 LAK cells from CD44v7 KO mice showed a significant decre
4 LAK cells from different mouse strains responded to Q9,
5 LAK cells generated from mice deficient in both perforin
6 LAK cells with genetically disrupted AdoRA2A were resist
9 , and TNF-beta) release by both TALL-104 and LAK cells, ligation of CD38L was not followed by cytokin
10 much lower levels than granzyme A in CTL and LAK cells, but its expression is unaltered in granzyme A
11 s report, however, we show that mouse NK and LAK cells and NK cell clones express full-length transcr
15 nd macrophage inflammatory protein-1alpha by LAK cells stimulated by cross-linking of the Ly49D recep
25 mes C, D, and F are also highly expressed in LAK cells, but minimally in cytotoxic T lymphocytes (CTL
26 e (NECA) (AdoRA2A/ADoRA2B agonist) inhibited LAK cell cytotoxicity in parallel with their ability to
27 40403 increased lymphokine-activated killer (LAK) cell cytotoxicity in vitro and in vivo, through inh
28 d cytotoxicity, lymphokine-activated killer (LAK) cell number and activity, and stimulated interleuki
29 ural killer and lymphokine-activated killer (LAK) cell-mediated cytotoxicity for G-CSF-mobilized effe
31 xic activity of lymphokine-activated killer (LAK) cells and determined whether both these effects are
32 Contact between lymphokine-activated killer (LAK) cells and natural killer-resistant tumor targets SK
34 with autologous lymphokine-activated killer (LAK) cells in seven patients with PTLD (four EBV-positiv
36 ral killer (NK)/lymphokine-activated killer (LAK) cells use perforin and/or Fas ligand (FasL) to medi
38 r (NK) cells or lymphokine-activated killer (LAK) cells, because they could kill neither NK cell-sens
42 liver, lymphokine-activated natural killer (LAK) cells were cocultured with Listeria-infected hepato
43 2-activated NK (lymphokine-activated killer (LAK)) cells, all splenic and liver NK cells, and approxi
44 into NK-like "lymphokine-activated killers" (LAK cells) under high doses of IL2 (a substitute for IL1
45 dministration of third-party non-HLA-matched LAK cells also to be effective in reducing tumor burden.
48 ADO strongly inhibited cytotoxic activity of LAK cells and attenuated the production of IFN-gamma, gr
52 ve with both mAbs, whereas the reactivity of LAK cells for IB4 and Moon-1 ranged from 10 to 60% among
53 These findings suggest that the response of LAK cells to infected hepatocytes may play a critical ro
56 , mimicked the inhibitory effects of CADO on LAK cell cytotoxic activity and cytokine production.
57 dy suggests that the expression of CD44v7 on LAK cells plays a specific role in EC injury and that it
59 -2K(b)-expressing B78H1 targets also reduced LAK cell activity, while H-2D(b) offered no protection.
62 ivated protein kinase kinase family member T-LAK cell-originated protein kinase (TOPK/PBK) is heavily
64 ed that NK1.1(+)TCR(-) NK and NK1.1(+)TCR(+) LAK cells were the prevalent cytolytic populations inhib
66 SV40 TAg was specifically expressed in the LAK cells of these mice, but not in resting T or NK cell
67 se data correlated with the finding that the LAK cells from IL-2-injected mice caused increased cytot
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