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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
7 A single dose of 5.2 x 10(9) to 5.6 x 10(10) LAK cells was given intravenously.
8                Interestingly, IL-2-activated LAK cells expressing CD44hi but not CD44lo were responsi
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
12          A role for natural killer (NK)- and LAK-cell-mediated killing is suggested because IL-2-prim
13 ing AdoR agonists and antagonists as well as LAK cells generated from AdoR knockout mice.
14                    In conclusion, autologous LAK cell infusion was effective for treatment of four EB
15 nd macrophage inflammatory protein-1alpha by LAK cells stimulated by cross-linking of the Ly49D recep
16               CD44v7-mediated lysis of EC by LAK cells was dependent on the activity of phosphatidyli
17 und that CHQ prevents perforin processing by LAK cells in vitro.
18                      IFN-gamma production by LAK cells was modulated by interleukin (IL)-2 and IL-12.
19 hanced the cytotoxicity of TALL-104 and CD8+ LAK cells against a resistant tumor target.
20            Human lymphokine-activated cells (LAK cells) and interferon alpha (IFN-alpha) have been us
21            In conclusion, T cells, NK cells, LAK cells, and their supernatants activated mycobacteric
22                     In parallel experiments, LAK cells reduced the tumorigenicity of a lymphoblastoid
23                             However, PKO/gld LAK cells were cytotoxic in long term cytotoxicity assay
24           Adenosine and its analogues impair LAK cell function by interfering with both perforin-medi
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
30 ial step during lymphokine-activated killer (LAK) cell-mediated cytotoxicity.
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
33                 Lymphokine-activated killer (LAK) cells generated from perforin knockout mice possess
34 with autologous lymphokine-activated killer (LAK) cells in seven patients with PTLD (four EBV-positiv
35  the ability of lymphokine-activated killer (LAK) cells to kill tumor cells.
36 ral killer (NK)/lymphokine-activated killer (LAK) cells use perforin and/or Fas ligand (FasL) to medi
37 killer (NK) and lymphokine-activated killer (LAK) cells were compared.
38 r (NK) cells or lymphokine-activated killer (LAK) cells, because they could kill neither NK cell-sens
39 otoxicity mediated by IL-2-activated killer (LAK) cells.
40 m lysis by bulk lymphokine-activated killer (LAK) cells.
41          Lymphokine (IL-2)-activated-killer (LAK) cells were capable of activating monocytes to kill
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.
46  progenitor compartment and to activated NK (LAK) cells.
47       There was dose-dependent inhibition of LAK cell-mediated cytotoxicity, but this effect was not
48 ADO strongly inhibited cytotoxic activity of LAK cells and attenuated the production of IFN-gamma, gr
49 iciently inhibited the cytotoxic activity of LAK cells.
50 104 (CD3/TCR-alphabeta+, CD8+, CD56+) and of LAK cells (90% CD3+).
51                               The effects of LAK cells and IFN-alpha therapy were examined in a sever
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
54                Interestingly, stimulation of LAK cells via NKG2D alone does not lead to cytokine rele
55 R2A in the inhibitory effect of adenosine on LAK cell cytotoxicity.
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
58             The effect of AdoR engagement on LAK cells cytotoxic activity was analyzed using AdoR ago
59 -2K(b)-expressing B78H1 targets also reduced LAK cell activity, while H-2D(b) offered no protection.
60                             IL-15-stimulated LAK cells induced a significant lytic response against t
61                                            T-LAK cell-originated protein kinase (TOPK) is expressed w
62 ivated protein kinase kinase family member T-LAK cell-originated protein kinase (TOPK/PBK) is heavily
63              PBK/TOPK (PDZ-binding kinase, T-LAK-cell-originated protein kinase) is a serine-threonin
64 ed that NK1.1(+)TCR(-) NK and NK1.1(+)TCR(+) LAK cells were the prevalent cytolytic populations inhib
65  inhibition assays suggested NK- rather than LAK-cell-mediated killing.
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
68                                        Thus, LAK cells are armed with at least three cytotoxic molecu
69                             Experiments with LAK cells derived from H2(b) SCID and B6 mice establishe
70                                 Studies with LAK cells generated from AdoRA1-/- and AdoRA3-/- mice ru

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