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Research Article Free access | 10.1172/JCI114984

Lack of HLA class I antigen expression by cultured melanoma cells FO-1 due to a defect in B2m gene expression.

C M D'Urso, Z G Wang, Y Cao, R Tatake, R A Zeff, and S Ferrone

Department of Microbiology and Immunology, New York Medical College, Valhalla 10595.

Find articles by D'Urso, C. in: JCI | PubMed | Google Scholar

Department of Microbiology and Immunology, New York Medical College, Valhalla 10595.

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Department of Microbiology and Immunology, New York Medical College, Valhalla 10595.

Find articles by Cao, Y. in: JCI | PubMed | Google Scholar

Department of Microbiology and Immunology, New York Medical College, Valhalla 10595.

Find articles by Tatake, R. in: JCI | PubMed | Google Scholar

Department of Microbiology and Immunology, New York Medical College, Valhalla 10595.

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Department of Microbiology and Immunology, New York Medical College, Valhalla 10595.

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Published January 1, 1991 - More info

Published in Volume 87, Issue 1 on January 1, 1991
J Clin Invest. 1991;87(1):284–292. https://doi.org/10.1172/JCI114984.
© 1991 The American Society for Clinical Investigation
Published January 1, 1991 - Version history
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Abstract

The melanoma cell line FO-1 does not express HLA class I antigens and does not acquire them on the cell surface after incubation with IFN-gamma. Immunochemical studies showed that FO-1 cells synthesize HLA class I heavy chain, but do not synthesize beta 2-microglobulin (beta 2-mu). The latter abnormality is associated with lack of beta 2-mu mRNA which remains undetectable in FO-1 cells incubated with IFN-gamma. The defect was identified as a genetic lesion in the B2m gene, since DNA hybridization analysis detected a deletion of the first exon of the 5'-flanking region, and of a segment of the first intron of the B2m gene. HLA class I antigen expression was reconstituted on melanoma cells FO-1 after transfection with the wild-type mouse B2m gene, thereby confirming the abnormality of the endogenous B2m gene. The defect identified in FO-1 cells is distinct from that underlying the lack of HLA class I antigen expression by lymphoblastoid cells Daudi, but is remarkably similar to that causing lack of H-2 class I antigen expression by mouse lymphoblastoid cells R1 (TL-). These results suggest that genetic recombination in the 5' region of the B2m gene is a recurrent mechanism in B2m gene defects. In addition to contributing to our understanding of molecular abnormalities in HLA class I antigen expression by melanoma cells, FO-1 cells represent a useful model for analyzing the role of HLA class I antigens in the biology of melanoma cells and in their interaction with cells of the immune system.

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