Lack of HLA-class I antigens in human neuroblastoma cells: analysis of its relationship to TAP and tapasin expression
Autor: | M V, Corrias, M, Occhino, M, Croce, A, De Ambrosis, M P, Pistillo, P, Bocca, V, Pistoia, S, Ferrini |
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Rok vydání: | 2001 |
Předmět: |
Extracellular Matrix Proteins
Brain Neoplasms Blotting Western Histocompatibility Antigens Class I Genes myc Gene Expression Immunoglobulins Membrane Transport Proteins Antineoplastic Agents Nerve Tissue Proteins Antiporters Interferon-gamma Neuroblastoma ATP Binding Cassette Transporter Subfamily B Member 3 Antigens Surface Tumor Cells Cultured Humans ATP-Binding Cassette Transporters RNA Messenger ATP Binding Cassette Transporter Subfamily B Member 2 Immunoglobulin Heavy Chains beta 2-Microglobulin Gene Deletion |
Zdroj: | Tissue antigens. 57(2) |
ISSN: | 0001-2815 |
Popis: | We studied the constitutive and the interferon (IFN)-gamma-induced expression of HLA class I antigen heavy chain, beta2-microglobulin (beta2m), TAP-1, TAP-2 and tapasin in a panel of eleven neuroblastoma cell lines. Surface expression of HLA class I antigens was low in eight out of eight neuroblastoma cell lines bearing MYC-N amplification and/or 1p deletion, while two out of three neuroblastoma cell lines lacking these genetic alterations showed normal expression. IFN-gamma treatment restored HLA class I antigen surface expression in all neuroblastoma cell lines. Eight out of 11 neuroblastoma cell lines did not express TAP-1 mRNA and three of them also lacked TAP-2 mRNA. beta2 m mRNA was barely detectable or absent in five neuroblastoma cell lines, while tapasin mRNA was always expressed. IFN-gamma upregulated the expression of HLA class I heavy chain, beta2 m, TAP-1, TAP-2 and tapasin, as detected at mRNA or protein level. Post-transcriptional events were involved in altered TAP-1 and beta2 m expression in one peculiar neuroblastoma cell line. These data indicate that multiple mechanisms play a role in the HLA class I antigen-deficient phenotype of human neuroblastoma. |
Databáze: | OpenAIRE |
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