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Your search keyword '"Lunt, Sarah Jane"' showing total 23 results
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23 results on '"Lunt, Sarah Jane"'

12. Abstract A57: Differential tumor cell expression of VEGF isoforms impacts on the tumor microenvironment, metastasis and radiation response in a mouse fibrosarcoma model

Author

English, William R., primary, Lunt, Sarah Jane, additional, Fisher, Matthew, additional, Hurrell, Jack E., additional, Lefley, Diane V., additional, Mukherjee, Debayan, additional, Daniel, Rachel, additional, Lyons, Scott K., additional, Kanthou, Chryso, additional, and Tozer, Gillian M., additional

Published
2015
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23. Utilizing the adjuvant proper ties of CD1d-dependent NK T cells in T cell-mediated immunotherapy.

Author

Silk, Jonathan D., Hermans, Ian F., Gileadi, Uzi, Tsung Wen Chong, Shepherd, Dawn, Salio, Mariolina, Mathew, Bini, Schmidt, Richard R., Lunt, Sarah Jane, Williams, Kaye J., Stratford, Ian J., Harris, Adrfan L., and Cerundolo, Vincenzo

Subjects
*T cells, *CELLULAR immunity, *IMMUNOTHERAPY, *GLYCOLIPIDS, *INTERFERONS, *IMMUNOLOGY
Abstract

Activation of invariant CD 1d-dependent NK T cells (iNKT cells) in vivo through administration of the glycolipid ligand α-galactosylceramide (αt-GalCer) or the sphingo sine-truncated α-GalCer analog OCH leads to CD40 signaling as well as the release of soluble molecules including type I andy interferons that contribute to DC maturation. This process enhances T cell immunity to antigens presented by the DC. The adjuvant activity is further amplified if APCs are stimulated through Toll-like receptor 4, suggesting that INKT cell signals can amplify maturation induced by microbial stimuli. The adjuvant activity of α-GalCer enhances both priming and boosting of CD8 T cells to coadministered peptide or protein antigens, including a peptide encoding the clinically relevant, HLA-A2-restricted epitope of the human tumor antigen NY-ESO-1. Importantly, α-GalCer was used to induce CD8+ T cells to antigens delivered orally, despite the fact that this route of administration is normally associated with blunted responses. Only T cell responses induced in the presence of INKT cell stimulation, whether by the i.v. or oral route, were capable of eradicating established tumors. Together these data highlight the therapeutic potential of INKT cell ligands in vaccination strategies, particularly "heterologous prime-boost" strategies against tumors, and provide evidence that INKT cell stimulation may be exploited in the development of oral vaccines. [ABSTRACT FROM AUTHOR]

Published
2004
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