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[Cancer Research 51, 27-32, January 1, 1991]
© 1991 American Association for Cancer Research

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Expression of Class I Major Histocompatibility Complex Antigens in Epstein-Barr Virus-carrying Lymphoblastoid Cell Lines and Burkitt Lymphoma Cells1

Wolfgang Jilg2, Raymond Voltz, Christine Markert-Hahn, Helga Mairhofer, Iris Münz and Hans Wolf

Max von Pettenkofer-Institute for Hygiene and Medical Microbiology, University of Munich, Munich, Federal Republic of Germany

Epstein-Barr virus (EBV) carrying lymphoblastoid cell lines (LCLs) and EBV-positive Burkitt lymphoma (BL) cells were compared for their expression of class I antigens of the major histocompatibility complex. Five common BL lines, LCLs, pokeweed mitogen-stimulated blasts and resting B-cells from healthy donors, and eight pairs of BL cells and LCLs, each pair originating from one patient, were tested. Quantitative analysis was performed using a radioimmunoassay; qualitative aspects were studied by one- and two-dimensional gel electrophoresis. In general, LCLs expressed significantly higher amounts of class I antigens than BL cells, the latter showing class I densities similar to or lower than peripheral resting B-cells. From analysis of the expression of class I-specific RNA, there is some evidence that class I antigen expression is regulated on the transcriptional level. In two BL cells studied, class I expression could be enhanced by {gamma}-interferon, whereas the corresponding LCLs seemed to be refractory to this treatment. One- and two-dimensional gel electrophoresis showed that in some BL lines, in addition to the generally lower class I expression, distinct class I specificities were down-regulated. None of these alterations in class I expression was EBV specific; however, they may well play a role in the recognition of BL cells and LCLs by cellular immune mechanisms. Thus, down-regulation of class I antigens may contribute to the resistance of BL cells to cytotoxic T-lymphocytes, whereas their enhanced expression may improve the recognition of EBV-infected LCLs.

1 This study was supported by a grant from the Deutsche Forschungsgemeinschaft, Sonderforschungsbereich 217, Project B 3 (H. W., W. J.).

2 To whom requests for reprints should be addressed, at Max von Pettenkofer Institute, University of Munich, Pettenkoferstrasse 9a, 8000 Munich 2, FRG.

Received 7/24/90. Accepted 9/26/90.




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C. G. Tepper and M. F. Seldin
Modulation of Caspase-8 and FLICE-Inhibitory Protein Expression as a Potential Mechanism of Epstein-Barr Virus Tumorigenesis in Burkitt's Lymphoma
Blood, September 1, 1999; 94(5): 1727 - 1737.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Cancer Research Clinical Cancer Research
Cancer Epidemiology Biomarkers & Prevention Molecular Cancer Therapeutics
Molecular Cancer Research Cancer Prevention Research
Cancer Prevention Journals Portal Cancer Reviews Online
Annual Meeting Education Book Meeting Abstracts Online
Copyright © 1991 by the American Association for Cancer Research.