| Literature DB >> 35523889 |
Bindu Varghese1,2, Lydia Lynch1,3, Lianne E Vriend1, Dobrin Draganov4,5, Justice M Clark1, Haydn T Kissick1,6, Sharlin Varghese7, Martin G Sanda1,6, Glenn Dranoff4,8, M Simo Arredouani1,9, Steven P Balk10, Mark A Exley11,12,13,14,15.
Abstract
Invariant natural killer T cells (iNKT cells) express a semi-invariant T cell receptor that recognizes certain glycolipids (including α-galactosylceramide, αGC) bound to CD1d, and can induce potent antitumor responses. Here, we assessed whether αGC could enhance the efficacy of a GM-CSF-producing tumor cell vaccine in the transgenic SV40 T antigen-driven TRAMP prostate cancer model. In healthy mice, we initially found that optimal T cell responses were obtained with αGC-pulsed TRAMP-C2 cells secreting GM-CSF and milk fat globule epidermal growth factor protein-8 (MFG-E8) with an RGD to RGE mutation (GM-CSF/RGE TRAMP-C2), combined with systemic low dose IL-12. In a therapeutic model, transgenic TRAMP mice were then castrated at ~ 20 weeks, followed by treatment with the combination vaccine. Untreated mice succumbed to tumor by ~ 40 weeks, but survival was markedly prolonged by vaccine treatment, with most mice surviving past 80 weeks. Prostates in the treated mice were heavily infiltrated with T cells and iNKT cells, which both secreted IFNγ in response to tumor cells. The vaccine was not effective if the αGC, IL-12, or GM-CSF secretion was eliminated. Finally, immunized mice were fully resistant to challenge with TRAMP-C2 cells. Together these findings support further development of therapeutic vaccines that exploit iNKT cell activation.Entities:
Keywords: CD1d; GM-CSF; Invariant NKT cell; Prostate cancer; Tumor vaccine; α-Galactosylceramide
Year: 2022 PMID: 35523889 DOI: 10.1007/s00262-022-03210-8
Source DB: PubMed Journal: Cancer Immunol Immunother ISSN: 0340-7004 Impact factor: 6.630