ArticleMolecular cancer2009
Identification of iGb3 and iGb4 in melanoma B16F10-Nex2 cells and the iNKT cell-mediated antitumor effect of dendritic cells primed with iGb3.
Article in Molecular cancer, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 17 citations in OpenAlex.
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- A limitless Brazilian scientist: Professor Travassos and his contribution to cancer biology.Brazilian journal of microbiology : [publication of the Brazilian Society for Microbiology] · 2023Review
- Natural Killer T and Natural Killer Cell-Based Immunotherapy Strategies Targeting Cancer.Biomolecules · 2023Review
- Epigenetic control ofFrontiers in immunology · 2023Article
- Invariant Natural Killer T Cells in Immune Regulation of Blood Cancers: Harnessing Their Potential in Immunotherapies.Frontiers in immunology · 2017Review
- TLR4-mediated immunomodulatory properties of the bacterial metalloprotease arazyme in preclinical tumor models.Oncoimmunology · 2016Article
- Identification of self-lipids presented by CD1c and CD1d proteins.The Journal of biological chemistry · 2011Article
- A semi-invariant Vα10+ T cell antigen receptor defines a population of natural killer T cells with distinct glycolipid antigen-recognition properties.Nature immunology · 2011Article
- Immunologic mapping of glycomes: implications for cancer diagnosis and therapy.Frontiers in bioscience (Scholar edition) · 2011Review
- iNKT cell autoreactivity: what is 'self' and how is it recognized?Nature reviews. Immunology · 2010Review
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
backgroundCD1d-restricted iNKT cells are protective against murine melanoma B16F10-Nex2 growing subcutaneously in syngeneic C57Bl/6 mice as inferred from the fast tumor development in CD1d-KO in comparison with wild type animals. CD1d glycoproteins are related to the class I MHC molecules, and are involved in the presentation, particularly by dentritic cells (DC), of lipid antigens to iNKT cells. In the present work we attempted to identify the endogenous lipid mediator expressed in melanoma cells inducing such immunesurveillance response and study the possibility of protecting animals challenged with tumor cells with lipid-primed DC.
resultsCrude cytosolic and membrane fractions from in vivo growing melanoma contained iNKT-stimulating substances. Lipids were then extracted from these cells and one of the fractions (i.e. F3A) was shown to prime bone marrow-derived dendritic cells (BMDC) to stimulate iNKT murine hybridoma (DN32D3) cells to produce IL-2. The active fraction was analyzed by electrospray ionization-mass spectrometry (ESI-LIT-MS) and both iGb3 and iGb4 were identified along with GM3. When iGb3 was incubated with BMDC and tested with DN32D3 cells, IL-2 was equally produced indicating iNKT cell activation. GM3 consistently inhibited this response. To assess the antitumor response-induced by iGb3, a cytotoxicity assay in vitro was used with [3H]-thymidine labeled B16F10-Nex2 cells. At target/effector (iGb3-activated iNKT) cell ratio of 100(-1)-100(-4) tumor cell lysis was shown. The antitumor activity in vivo was tested in mice challenged i.v. with B16F10-Nex2 cells and treated with iGb3- or alpha-galactosylceramide-primed DCs. A 4-fold lower tumor load in the lungs was observed with either treatment.
conclusionOur results show the expression of globo and isoglobohexosylceramides in murine melanoma B16F10-Nex2. The expression of iGb3 and its precursor, iGb4, on tumor cells may prime an effective iNKT cell-dependent antitumor response, modulated negatively by GM3 which is also produced in these cells. iGb3-primed BMDC exerted a significant iNKT cell-mediated anti-tumor activity in mice challenged with melanoma cells.
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