Characterization of HLA class I altered phenotypes in a panel of human melanoma cell lines

Background Altered HLA class I cell surface expression is one of the major mechanisms by which tumor cells escape from T lymphocytes. Immunohistochemistry-defined phenotypes of lost HLA class I expression have been described in human solid tumors, nut less information is available on melanoma cell l...

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Veröffentlicht in:Cancer Immunology, Immunotherapy Immunotherapy, 2008-05, Vol.57 (5), p.719-729
Hauptverfasser: Méndez, Rosa, Rodríguez, Teresa, Del Campo, Ana, Monge, Eva, Maleno, Isabel, Aptsiauri, Natalia, Jiménez, Pilar, Pedrinaci, Susana, Pawelec, Graham, Ruiz-Cabello, Francisco, Garrido, Federico
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Sprache:eng
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Zusammenfassung:Background Altered HLA class I cell surface expression is one of the major mechanisms by which tumor cells escape from T lymphocytes. Immunohistochemistry-defined phenotypes of lost HLA class I expression have been described in human solid tumors, nut less information is available on melanoma cell lines. Objectives To describe the frequency and distribution of different types of HLA class I antigen alterations in 91 melanoma cell lines from the European Searchable Tumour Cell and Databank (ESTDAB). Methods The HLA class I expression was assessed by flow cytometry and HLA genotyping. Results We found various types of HLA class I cell surface alterations in about 67% of the melanoma cell lines. These alterations range from total to selective HLA class I loss due to loss of heterozygosity (LOH), haplotype loss, β2-microglobulin gene mutation, and/or total or selective down-regulation of HLA class I molecules. The most frequently observed phenotype is down-regulation of HLA-B locus that was reversible after treatment with IFN -γ. Conclusions In general, HLA class I alterations in the majority of the cells analyzed were of regulatory nature and could be restored by IFN-γ. Analysis of the frequency of distinct HLA class I altered phenotypes in these melanoma cell lines revealed specific differences compared to other types of tumors.
ISSN:0340-7004
1432-0851
DOI:10.1007/s00262-007-0411-3