Toll-like receptor agonists and invariant natural killer T-cells enhance antibody-dependent cell-mediated cytotoxicity (ADCC)

被引：23

作者：

Moreno, Maria ^{[1
,2
]}

Mol, Berber M. ^{[1
]}

von Mensdorff-Pouilly, Silvia ^{[2
]}

Verheijen, Rene H. M. ^{[3
]}

von Blomberg, B. Mary E. ^{[1
]}

van den Eertwegh, Alfons J. M. ^{[4
]}

Scheper, Rik J. ^{[1
]}

Bontkes, Hetty J. ^{[1
]}

机构：

[1] Vrije Univ Amsterdam Med Ctr, Dept Pathol, NL-1081 HV Amsterdam, Netherlands

[2] Vrije Univ Amsterdam Med Ctr, Dept Obstet & Gynaecol, NL-1081 HV Amsterdam, Netherlands

[3] Univ Med Ctr Utrecht, Dept Woman & Baby, Div Surg & Oncol Gynaecol, Utrecht, Netherlands

[4] Vrije Univ Amsterdam Med Ctr, Dept Med Oncol, NL-1081 HV Amsterdam, Netherlands

来源：

CANCER LETTERS | 2008年 / 272卷 / 01期

关键词：

Human; Invariant NKT cells; Toll-like receptors; NK cells; ADCC;

D O I：

10.1016/j.canlet.2008.06.028

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

huHMFG-1 (AS1402) is a humanised IgG1 against MUC1, which exerts tumour cell killing through antibody-dependent cellular cytotoxicity (ADCC) mediated by natural killer (NK) cells. Here, we explored the capacity of invariant NKT (iNKT) cells, which are known to activate NK cells, and toll-like receptor (TLR) ligands which activate both iNKT and NK cells, to enhance huHMFG-1-ADCC. Addition of iNKT cells, as well as TLR2/6, 7, 8 and 9 agonists to PBMC improved the efficacy of huHMFG-1. These results suggest that transfer of ex vivo expanded iNKT cells or TLR agonist treatment may improve the efficacy of NK cell-mediated antibody-based tumour immunotherapies. (C) 2008 Elsevier Ireland Ltd. All rights reserved.

引用

页码：70 / 76

页数：7

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