Expression of Epstein-Barr Virus Nuclear Antigen 1 Is Associated with Enhanced Expression of CD25 in the Hodgkin Cell Line L428-Reference-Cited by-同舟云学术

Expression of Epstein-Barr Virus Nuclear Antigen 1 Is Associated with Enhanced Expression of CD25 in the Hodgkin Cell Line L428

Published:1999-02 Issue:2 Volume:73 Page:1630-1636
ISSN:0022-538X
Container-title:Journal of Virology
language:en
Short-container-title:J Virol

Author:

Kube D.¹²,Vockerodt M.¹²,Weber O.³,Hell K.⁴,Wolf J.¹,Haier B.¹,Grässer F. A.⁵,Müller-Lantzsch N.⁵,Kieff E.⁶,Diehl V.¹,Tesch H.¹

Affiliation:

1. Klinik für Innere Medizin I,1

2. Zentrum für Molekulare Medizin der Universität Köln,2 and

3. Bayer AG, Wuppertal,3 Germany, and

4. Institut für Pathologie der Universität Köln,4 Cologne,

5. Institut für Virologie der Universität Homburg, Homburg,5 and

6. Department of Medicine and Microbiology and Molecular Genetics, Harvard Medical School, Boston, Massachusetts6

Abstract

ABSTRACT Epstein-Barr virus is associated with several human malignancies including Burkitt’s lymphoma, nasopharyngeal carcinoma, and Hodgkin’s disease (HD). To examine the effect of Epstein-Barr virus nuclear antigen 1 (EBNA-1) in the pathogenesis of HD, we transfected the gene into the HD cell line L428. EBNA-1 expression was associated with significantly enhanced CD25 expression (interleukin 2 [IL-2]-receptor α chain) in transient and stably transfected L428 cells but did not affect the expression of IL-2 receptor β and γ chains. There was no up-regulation of the B-cell activation molecules CD23, CD30, CD39, CD40, CD44, CD71, and CD54 (intercellular adhesion molecule 1) or enhanced production of IL-6, IL-10, lymphotoxin alpha, and the soluble form of CD25. Stable EBNA-1-expressing L428 cells were nontumorigenic in SCID mice but showed enhanced lymphoma development in nonobese diabetic-SCID mice compared to mock-transfected cells.

Publisher

American Society for Microbiology

Subject

Virology,Insect Science,Immunology,Microbiology

Link

https://journals.asm.org/doi/pdf/10.1128/JVI.73.2.1630-1636.1999

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