A melanoma immune response signature including Human Leukocyte Antigen-E

Elisa Tremante; Agnese Ginebri; Elisa Lo Monaco; Barbara Benassi; Pasquale Frascione; Paola Grammatico; Sandra Cappellacci; Caterina Catricalà; Diego Arcelli; Pier Giorgio Natali; Franco Di Filippo; Marcella Mottolese; Paolo Visca; Maria Benevolo; Patrizio Giacomini

doi:10.1111/pcmr.12164

A melanoma immune response signature including Human Leukocyte Antigen-E

Elisa Tremante, Agnese Ginebri, Elisa Lo Monaco, Barbara Benassi, Pasquale Frascione, Paola Grammatico, Sandra Cappellacci, Caterina Catricalà, Diego Arcelli, Pier Giorgio Natali, Franco Di Filippo, Marcella Mottolese, Paolo Visca, Maria Benevolo, Patrizio Giacomini

Research output: Contribution to journal › Article › peer-review

Abstract

Paired cultures of early-passage melanoma cells and melanocytes were established from metastatic lesions and the uninvolved skin of five patients. In this stringent autologous setting, cDNA profiling was used to analyze a subset of 1477 genes selected by the Gene Ontology term 'immune response'. Human Leukocyte Antigen E (HLA-E) was ranked 19th among melanoma-overexpressed genes and was embedded in a transformation signature including its preferred peptide ligand donors HLA-A, HLA-B, HLA-C, and HLA-G. Mostly undetectable in normal skin and 39 nevi (including rare and atypical lesions), HLA-E was detected by immunohistochemistry in 17/30 (57%) and 32/48 (67%) primary and metastatic lesions, respectively. Accordingly, surface HLA-E was higher on melanoma cells than on melanocytes and protected the former (6/6 cell lines) from lysis by natural killer (NK) cells, functionally counteracting co-expressed triggering ligands. Although lacking HLA-E, melanocytes (4/4 cultures) were nevertheless (and surprisingly) fully protected from NK cell lysis.

Original language	English
Pages (from-to)	103-112
Number of pages	10
Journal	Pigment Cell and Melanoma Research
Volume	27
Issue number	1
DOIs	https://doi.org/10.1111/pcmr.12164
Publication status	Published - Jan 2014

Keywords

cDNA arrays
HLA-E
Melanocytes
Melanoma
NK cells

ASJC Scopus subject areas

Dermatology
Oncology
Biochemistry, Genetics and Molecular Biology(all)

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Tremante, E., Ginebri, A., Lo Monaco, E., Benassi, B., Frascione, P., Grammatico, P., Cappellacci, S., Catricalà, C., Arcelli, D., Natali, P. G., Di Filippo, F., Mottolese, M., Visca, P., Benevolo, M., & Giacomini, P. (2014). A melanoma immune response signature including Human Leukocyte Antigen-E. Pigment Cell and Melanoma Research, 27(1), 103-112. https://doi.org/10.1111/pcmr.12164

A melanoma immune response signature including Human Leukocyte Antigen-E. / Tremante, Elisa; Ginebri, Agnese; Lo Monaco, Elisa; Benassi, Barbara; Frascione, Pasquale; Grammatico, Paola; Cappellacci, Sandra; Catricalà, Caterina; Arcelli, Diego; Natali, Pier Giorgio; Di Filippo, Franco; Mottolese, Marcella ; Visca, Paolo ; Benevolo, Maria ; Giacomini, Patrizio.

In: Pigment Cell and Melanoma Research, Vol. 27, No. 1, 01.2014, p. 103-112.

Research output: Contribution to journal › Article › peer-review

Tremante, E, Ginebri, A, Lo Monaco, E, Benassi, B, Frascione, P, Grammatico, P, Cappellacci, S, Catricalà, C, Arcelli, D, Natali, PG, Di Filippo, F, Mottolese, M , Visca, P , Benevolo, M & Giacomini, P 2014, 'A melanoma immune response signature including Human Leukocyte Antigen-E', Pigment Cell and Melanoma Research, vol. 27, no. 1, pp. 103-112. https://doi.org/10.1111/pcmr.12164

Tremante, Elisa ; Ginebri, Agnese ; Lo Monaco, Elisa ; Benassi, Barbara ; Frascione, Pasquale ; Grammatico, Paola ; Cappellacci, Sandra ; Catricalà, Caterina ; Arcelli, Diego ; Natali, Pier Giorgio ; Di Filippo, Franco ; Mottolese, Marcella ; Visca, Paolo ; Benevolo, Maria ; Giacomini, Patrizio. / A melanoma immune response signature including Human Leukocyte Antigen-E. In: Pigment Cell and Melanoma Research. 2014 ; Vol. 27, No. 1. pp. 103-112.

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abstract = "Paired cultures of early-passage melanoma cells and melanocytes were established from metastatic lesions and the uninvolved skin of five patients. In this stringent autologous setting, cDNA profiling was used to analyze a subset of 1477 genes selected by the Gene Ontology term 'immune response'. Human Leukocyte Antigen E (HLA-E) was ranked 19th among melanoma-overexpressed genes and was embedded in a transformation signature including its preferred peptide ligand donors HLA-A, HLA-B, HLA-C, and HLA-G. Mostly undetectable in normal skin and 39 nevi (including rare and atypical lesions), HLA-E was detected by immunohistochemistry in 17/30 (57%) and 32/48 (67%) primary and metastatic lesions, respectively. Accordingly, surface HLA-E was higher on melanoma cells than on melanocytes and protected the former (6/6 cell lines) from lysis by natural killer (NK) cells, functionally counteracting co-expressed triggering ligands. Although lacking HLA-E, melanocytes (4/4 cultures) were nevertheless (and surprisingly) fully protected from NK cell lysis.",

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N2 - Paired cultures of early-passage melanoma cells and melanocytes were established from metastatic lesions and the uninvolved skin of five patients. In this stringent autologous setting, cDNA profiling was used to analyze a subset of 1477 genes selected by the Gene Ontology term 'immune response'. Human Leukocyte Antigen E (HLA-E) was ranked 19th among melanoma-overexpressed genes and was embedded in a transformation signature including its preferred peptide ligand donors HLA-A, HLA-B, HLA-C, and HLA-G. Mostly undetectable in normal skin and 39 nevi (including rare and atypical lesions), HLA-E was detected by immunohistochemistry in 17/30 (57%) and 32/48 (67%) primary and metastatic lesions, respectively. Accordingly, surface HLA-E was higher on melanoma cells than on melanocytes and protected the former (6/6 cell lines) from lysis by natural killer (NK) cells, functionally counteracting co-expressed triggering ligands. Although lacking HLA-E, melanocytes (4/4 cultures) were nevertheless (and surprisingly) fully protected from NK cell lysis.

AB - Paired cultures of early-passage melanoma cells and melanocytes were established from metastatic lesions and the uninvolved skin of five patients. In this stringent autologous setting, cDNA profiling was used to analyze a subset of 1477 genes selected by the Gene Ontology term 'immune response'. Human Leukocyte Antigen E (HLA-E) was ranked 19th among melanoma-overexpressed genes and was embedded in a transformation signature including its preferred peptide ligand donors HLA-A, HLA-B, HLA-C, and HLA-G. Mostly undetectable in normal skin and 39 nevi (including rare and atypical lesions), HLA-E was detected by immunohistochemistry in 17/30 (57%) and 32/48 (67%) primary and metastatic lesions, respectively. Accordingly, surface HLA-E was higher on melanoma cells than on melanocytes and protected the former (6/6 cell lines) from lysis by natural killer (NK) cells, functionally counteracting co-expressed triggering ligands. Although lacking HLA-E, melanocytes (4/4 cultures) were nevertheless (and surprisingly) fully protected from NK cell lysis.

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A melanoma immune response signature including Human Leukocyte Antigen-E

Abstract

Keywords

ASJC Scopus subject areas

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