title: Gap junction communication between autologous endothelial and tumor cells induce cross-recognition and elimination by specific CTL.
abstract: Cellular interactions in the tumor stroma play a major role in cancer progression but can also induce tumor rejection. To explore the role of endothelial cells in these interactions, we used an in vitro three-dimensional collagen matrix model containing a cytotoxic T lymphocyte CTL clone (M4.48), autologous tumor cells (M4T), and an endothelial cell (M4E) line that are all derived from the same tumor. We demonstrate in this study that specific killing of the endothelial cells by the CTL clone required the autologous tumor cells and involved Ag cross-presentation. The formation of gap junctions between endothelial and tumor cells is required for antigenic peptide transfer to endothelial cells that are then recognized and eliminated by CTL. Our results indicate that gap junctions facilitate an effective CTL-mediated destruction of endothelial cells from the tumor microenvironment that may contribute to the control of tumor progression.
authors.affiliation: Institut National de la Santé et de la Recherche Médicale Unite 753, Institut Fédératif de Recherche 54, Villejuif, France.
authors.forename: Houssem
authors.initials: H
authors.lastname: Benlalam
authors.forename: Abdelali
authors.initials: A
authors.lastname: Jalil
authors.forename: Meriem
authors.initials: M
authors.lastname: Hasmim
authors.forename: Baoxu
authors.initials: B
authors.lastname: Pang
authors.forename: Ryad
authors.initials: R
authors.lastname: Tamouza
authors.forename: Michèle
authors.initials: M
authors.lastname: Mitterrand
authors.forename: Yann
authors.initials: Y
authors.lastname: Godet
authors.forename: Nathalie
authors.initials: N
authors.lastname: Lamerant
authors.forename: Caroline
authors.initials: C
authors.lastname: Robert
authors.forename: Marie-Françoise
authors.initials: MF
authors.lastname: Avril
authors.forename: Jacques
authors.initials: J
authors.lastname: Neefjes
authors.forename: Thomas
authors.initials: T
authors.lastname: Tursz
authors.forename: Fathia
authors.initials: F
authors.lastname: Mami-Chouaib
authors.forename: Claudine
authors.initials: C
authors.lastname: Kieda
authors.forename: Salem
authors.initials: S
authors.lastname: Chouaib
mesh_terms: D000951:Antigens, Neoplasm / Q000378:metabolism; D015415:Biomarkers / Q000378:metabolism; D014408:Biomarkers, Tumor / Q000378:metabolism; D002450:Cell Communication / Q000276:immunology*; D045744:Cell Line, Tumor; D002999:Clone Cells; D018920:Coculture Techniques; D045142:Cross-Priming / Q000276:immunology*; D003600:Cytosol / Q000276:immunology / Q000378:metabolism; D003602:Cytotoxicity, Immunologic / Q000276:immunology; D042783:Endothelial Cells / Q000276:immunology* / Q000378:metabolism / Q000473:pathology*; D017629:Gap Junctions / Q000276:immunology* / Q000378:metabolism / Q000473:pathology; D006801:Humans; D016246:Lymphocytes, Tumor-Infiltrating / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D008545:Melanoma / Q000276:immunology* / Q000473:pathology* / Q000628:therapy; D013602:T-Lymphocytes, Cytotoxic / Q000276:immunology* / Q000378:metabolism / Q000473:pathology
chemical_list: D000951:Antigens, Neoplasm; D015415:Biomarkers; D014408:Biomarkers, Tumor