title: Variable expression on lung cancer cell lines of HLA-A2-binding MAGE-3 peptide recognized by cytotoxic T lymphocytes.
abstract: Cytotoxic T lymphocytes (CTL) specific for HLA-A2-binding MAGE-3 peptide (FLWGPRALV) were generated by repetitive stimulation of PBMC with the peptide in the presence of EBV-transformed B blasts and IL-2. Using these CTL, we investigated the expression of the HLA-A2-binding MAGE-3 peptide on lung cancer cell lines. Of 14 cell lines investigated, 1-87, PC-9, OU-LC-KI, 11-18 and LK87 were derived from HLA-A2 positive patients. But cytofluorometry analysis showed that 1-87, PC-9 and OU-LC-KI, but not 11-18 or LK87 expressed the HLA-A2 antigen. All five cell lines expressed MAGE-3 gene mRNA. Twelve of thirteen CTL lines from two HLA-A2 positive donors showed no cytotoxicity against any of the 14 lung cancer cell lines. CTL line TI-1 showed cytotoxicity against 1-87 but not against any of the other cell lines. Treatment of 1-87 with IFN-gamma greatly augmented the cytotoxicity of TI-1 and induced it in the other 12 CTL lines, confirming the expression of the peptide on 1-87. No cytotoxicity was induced by IFN-gamma treatment of PC-9 or OU-LC-KI. However, PC-9 and OU-LC-KI pulsed with the peptide were killed efficiently by all of the CTL lines, suggesting no expression of the peptide on those cells. A low level of cytotoxicity was induced on 11-18 but not LK87 by IFN-gamma treatment, although expression of the HLA-A2 antigen was not observed by cytofluorometry. These findings showed that expression of the HLA-A2-binding MAGE-3 peptide recognized by CTL was variable on lung cancer cell lines.
authors.affiliation: Department of Internal Medicine, Okayama University Medical School, 2-5-1 Shikata-cho, Okayama 700, Japan.
authors.forename: T
authors.initials: T
authors.lastname: Takaki
authors.forename: A
authors.initials: A
authors.lastname: Hiraki
authors.forename: A
authors.initials: A
authors.lastname: Uenaka
authors.forename: S
authors.initials: S
authors.lastname: Gomi
authors.forename: K
authors.initials: K
authors.lastname: Itoh
authors.forename: H
authors.initials: H
authors.lastname: Udono
authors.forename: A
authors.initials: A
authors.lastname: Shibuya
authors.forename: T
authors.initials: T
authors.lastname: Tsuji
authors.forename: S
authors.initials: S
authors.lastname: Sekiguchi
authors.forename: E
authors.initials: E
authors.lastname: Nakayama
mesh_terms: D000595:Amino Acid Sequence; D000951:Antigens, Neoplasm / Q000096:biosynthesis / Q000737:chemistry / Q000276:immunology; D003602:Cytotoxicity, Immunologic; D015789:HLA-A2 Antigen / Q000276:immunology* / Q000378:metabolism; D006801:Humans; D008175:Lung Neoplasms / Q000276:immunology*; D008213:Lymphocyte Activation; D009363:Neoplasm Proteins / Q000096:biosynthesis / Q000737:chemistry / Q000276:immunology*; D010446:Peptide Fragments / Q000737:chemistry / Q000276:immunology; D013602:T-Lymphocytes, Cytotoxic / Q000276:immunology*; D014407:Tumor Cells, Cultured
chemical_list: D000951:Antigens, Neoplasm; D015789:HLA-A2 Antigen; C072013:MAGEA3 protein, human; D009363:Neoplasm Proteins; D010446:Peptide Fragments