Skip to main content
  • Antigenic Profiling of Glioblastoma: Molecular analysis of the presentation of Melanoma-associated differentiation antigens-derived epitopes using recombinant antibodies mimicking T-cell receptor spec

    Final Number:
    678

    Authors:
    Or Cohen-Inbar; Inbal Zafir-Lavie; Yael Michaeli; Tali Voloshin; Hila Novak; Noa Ezaguy; Galit Denkberg; Pedro Romero; Menashe Zaaroor; Yoram Reiter Technion Israel Institute Of Technology

    Study Design:
    Laboratory Investigation

    Subject Category:

    Meeting: Congress of Neurological Surgeons 2014 Annual Meeting

    Introduction: Glioblastoma Multiforme (GBM) is the most common primary malignant tumor of the central nervous system. GBM patients manifest as immunosupressed both systemically and locally. Impaired humoral as well as cellular immunity with impaired local cytotoxic T-cell reaction and recruitment is known, due in part to the immunosuppressive nature of the tumor milieu. The immunoprofile of GBM is not well characterized. Although melanoma and GBM are both neuroectodermally originated tumors, sharing differentiation/other antigens, only the immune profile of melanoma has been well-characterized. In this study we characterized HLA-A2 restricted melanoma associated peptides presentation on GBM cell lines and solid tumor samples from GBM patients.

    Methods: RNA analysis, flow cytometry, Western blotting, mass spectroscopy and Cytotoxic T lymphocytes toxicity assay results were compared to those of immunohistochemistry with engineered antibodies bearing specificity of T-cell receptor constructed in this paper. These antibodies enable us to directly analyze HLA-A2 restricted peptides on cell surface of GBM and melanoma. Four melanoma associated differentiation antigens were targeted: MART-1, Tyrosinase, Gp100 and MAGE-A1.

    Results: The presentation of HLA-A2/MART-1(26-35, A27L) complexes on the surface of U-251MG GBM cell line was relatively low and that of the HLA-A2/gp-100(209-217, T210M) and HLA-A2/MAGE-A1(278-286) was moderate. HLA-A2/Tyrosinase(369-377) was presented in relatively high levels on GBM cell lines (a finding corroborated by mass spectrometry analysis) and was also present on human GBM tumor samples; this was inconsistent with our results from cytolytic T-cell assay which may suggest non-to-low presentation of HLA-A2/Tyrosinase(369-377) complex. This inconsistency probably stems from presentation levels which, albeit being relatively high, are not sufficient to enable effective lysis of target cells, particularly because the anti-Tyrosinase CTL clones have low avidity and therefore require higher antigen concentrations to effectively mediate lysis.

    Conclusions: Our profiling sheds light on the immunological profile of GBM and its evolution and may create new targets for immunotherapy.

    Patient Care: developing better understanding and immunotherapy for GBM

    Learning Objectives: developing better understanding and immunotherapy for GBM

    References:

We use cookies to improve the performance of our site, to analyze the traffic to our site, and to personalize your experience of the site. You can control cookies through your browser settings. Please find more information on the cookies used on our site. Privacy Policy