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Title: A new strategy to induce effective antitumour response in vitro and in vivo
Authors: Wang, M.
Xie, Z. 
Shi, M.
Lu, H.
Yu, M.
Hu, M.
Lu, F.
Ma, Y.
Shen, B.
Guo, N.
Issue Date: Sep-2008
Citation: Wang, M., Xie, Z., Shi, M., Lu, H., Yu, M., Hu, M., Lu, F., Ma, Y., Shen, B., Guo, N. (2008-09). A new strategy to induce effective antitumour response in vitro and in vivo. Scandinavian Journal of Immunology 68 (3) : 287-296. ScholarBank@NUS Repository.
Abstract: To induce Her2-specific cell immune response, we used xenogeneic antigen rat neu L2-S2 domains as the vaccine antigen. The antigenic protein was engineered as a chimeric protein with human IgG1 Fc region (neu-Fc). Neu-Fc could stimulate the cell proliferation in mixed lymphocyte reaction effectively. Simultaneous neu-Fc and IFN-γ stimulation dramatically elevated IL-12 secretion and reduced IL-10 production in PBMC. To further augment the activating effects on Th1-type response, Bacille Calmette-Guerin (BCG) was utilized as a non-specific stimulus. Neu-Fc, IFN-γ and BCG costimulation exhibited the most conspicuous effects on the reversal of the Th1-type inhibitory effects by MCF-7 cell supernatant compared with neu-Fc alone or IFN-γ and BCG costimulation. The lytic activity of effector cells to Her2 overexpressing cells was greatly promoted by neu-Fc, IFN-γ and BCG stimulation simultaneously. Neu-Fc led to considerable retardation in EMT6/Her2 tumour growth in Balb/c mice. IFN-γ and BCG efficiently enhanced the antitumour activity. A large amount of inflammatory cells were found to be accumulated in the tumour tissues or surrounded tumours in mice treated with neu-Fc, IFN-γ and BCG but no inflammatory cell infiltration was observed in control tumours, indicating that the strategy is potent enough to support the initiation and propagation of tumour-specific immune response in an established tumour and generate a proinflammatory environment. © 2008 The Authors.
Source Title: Scandinavian Journal of Immunology
ISSN: 03009475
DOI: 10.1111/j.1365-3083.2008.02140.x
Appears in Collections:Staff Publications

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