title: Presence of D110 antigen expressing immunocompetent cells in glioblastoma associates with prolonged survival.
abstract: Monoclonal antibody D110 has recently been described as a novel marker of hypoxic tissue damage, reacting with a so far unknown antigen with preferential expression in the central nervous system. The aim of the study was to investigate D110 immunoreactivity in glioblastoma, its association with the expression of hypoxia-related proteins and its impact on patient outcome. A total of 114 consecutive adult patients who underwent first operation of primary glioblastoma were included in this study. We evaluated D110 immunoreactivity qualitatively and semi-quantitatively and correlated it with expression of hypoxia inducible factor 1 alpha (HIF-1alpha), expression of vascular endothelial growth factor (VEGF), and with patient survival using univariate and multivariate statistical analysis. We observed D110 immunolabelling in 85.1% of the cases. D110 immunoreactivity was detectable in infiltrating HLA-DR and CD68 expressing cells, most likely microglial cells or haematogenous cells of monocyte/macrophage lineage. In the peripheral lymphoreticular system, immunohistochemistry disclosed selective D110 labelling of Langerhans cells and of dendritic cells of the thymic medulla. Univariate statistical analysis revealed significantly longer survival of patients whose glioblastomas contained D110 immunoreactive infiltrating cells. There was no association between presence of D110 immunoreactive cells and expression of HIF-1alpha and VEGF. We conclude that D110 immunoreactivity in glioblastoma does not seem to be related to tissue hypoxia. D110 identifies immunocompetent cells, which positively influence survival of glioblastoma patients.
authors.affiliation: Institute of Neurology, Medical University Vienna, Vienna, Austria.
authors.forename: M
authors.initials: M
authors.lastname: Preusser
authors.forename: T
authors.initials: T
authors.lastname: Ströbel
authors.forename: P
authors.initials: P
authors.lastname: Birner
authors.forename: C
authors.initials: C
authors.lastname: Marosi
authors.forename: K
authors.initials: K
authors.lastname: Dieckmann
authors.forename: K
authors.initials: K
authors.lastname: Rössler
authors.forename: H
authors.initials: H
authors.lastname: Budka
authors.forename: H
authors.initials: H
authors.lastname: Lassmann
authors.forename: J A
authors.initials: JA
authors.lastname: Hainfellner
mesh_terms: D000328:Adult; D000368:Aged; D000911:Antibodies, Monoclonal / Q000378:metabolism*; D015703:Antigens, CD / Q000276:immunology / Q000378:metabolism; D015214:Antigens, Differentiation, Myelomonocytic / Q000276:immunology / Q000378:metabolism; D000951:Antigens, Neoplasm / Q000276:immunology / Q000378:metabolism*; D001932:Brain Neoplasms / Q000378:metabolism* / Q000401:mortality / Q000473:pathology; D015331:Cohort Studies; D003713:Dendritic Cells / Q000276:immunology / Q000473:pathology; D005260:Female; D005455:Fluorescent Antibody Technique; D005909:Glioblastoma / Q000378:metabolism* / Q000401:mortality / Q000473:pathology; D006684:HLA-DR Antigens / Q000276:immunology / Q000378:metabolism; D006801:Humans; D051795:Hypoxia-Inducible Factor 1, alpha Subunit; D007121:Immunocompetence / Q000502:physiology*; D007150:Immunohistochemistry; D008208:Lymphatic System / Q000276:immunology / Q000473:pathology; D008297:Male; D008875:Middle Aged; D009457:Neuroglia / Q000276:immunology / Q000473:pathology; D012189:Retrospective Studies; D013534:Survival; D014157:Transcription Factors / Q000378:metabolism; D000097382:CD68 Molecule
chemical_list: D000911:Antibodies, Monoclonal; D015703:Antigens, CD; D015214:Antigens, Differentiation, Myelomonocytic; D000951:Antigens, Neoplasm; D006684:HLA-DR Antigens; D051795:Hypoxia-Inducible Factor 1, alpha Subunit; D014157:Transcription Factors; C067980:CD68 antigen, human; D000097382:CD68 Molecule; C497442:HIF1A protein, human