LMP-1, the Epstein-Barr virus-encoded oncogene with a B cell activating mechanism similar to CD40

被引:18
作者
Klein, E [1 ]
Teramoto, N
Gogolák, P
Nagy, N
Björkholm, M
机构
[1] Karolinska Inst, Microbiol & Tumorbiol Ctr, Stockholm, Sweden
[2] Karolinska Hosp, Dept Hematol, S-10401 Stockholm, Sweden
关键词
Epstein-Barr virus; lymphocytes; DNA;
D O I
10.1016/S0165-2478(99)00044-9
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Many details in the expression pattern of Epstein-Barr virus (EBV)-encoded proteins, their role in blast and growth transformation in infected B lymphocytes are known, but 'black holes' still exist. The two main types of virus-B lymphocyte interactions are denoted as Type I and Type III. These are characterized by the difference in the EBV protein expression which is related to the phenotype of the cell. The difference was first detected in comparisons between Burkitt lymphoma cells (BL) and lymphoblastoid cell lines, LCLs, which arise from normal B lymphocytes after experimental infection and are growth transformed by EBV. A third type of interaction can be seen in B-CLL cells which carry the EBV receptor CD21 and can be thus infected with the virus in vitro. The infected cells express the EBV-encoded proteins with a pattern which is different from the above mentioned two types, in that they express the nuclear proteins but not the membrane localized LMP-1. Importantly, the infected B-CLL cells do not enter DNA synthesis and they do not growth transform. Normal B lymphocytes with similar expression pattern have been seen in analysis of the lymphoreticular tissues of patients which responded to the primary EBV infection with development of the infectious mononucleosis symptoms. (C) 1999 Elsevier Science B.V. All rights reserved.
引用
收藏
页码:147 / 154
页数:8
相关论文
共 33 条
[21]   THE EPSTEIN-BARR-VIRUS TRANSFORMING PROTEIN LMP1 ENGAGES SIGNALING PROTEINS FOR THE TUMOR-NECROSIS-FACTOR RECEPTOR FAMILY [J].
MOSIALOS, G ;
BIRKENBACH, M ;
YALAMANCHILI, R ;
VANARSDALE, T ;
WARE, C ;
KIEFF, E .
CELL, 1995, 80 (03) :389-399
[22]   LONG-TERM T-CELL-MEDIATED IMMUNITY TO EPSTEIN-BARR VIRUS IN MAN .1. COMPLETE REGRESSION OF VIRUS-INDUCED TRANSFORMATION IN CULTURES OF SEROPOSITIVE DONOR LEUKOCYTES [J].
MOSS, DJ ;
RICKINSON, AB ;
POPE, JH .
INTERNATIONAL JOURNAL OF CANCER, 1978, 22 (06) :662-668
[23]  
Niedobitek G, 1997, J PATHOL, V182, P151, DOI 10.1002/(SICI)1096-9896(199706)182:2<151::AID-PATH824>3.0.CO
[24]  
2-3
[25]   THE ASSOCIATION OF EPSTEIN-BARR-VIRUS (EBV) WITH T-CELL LYMPHOPROLIFERATIONS AND HODGKINS-DISEASE - 2 NEW DEVELOPMENTS IN THE EBV FIELD [J].
PALLESEN, G ;
HAMILTONDUTOIT, SJ ;
ZHOU, XG .
ADVANCES IN CANCER RESEARCH, VOL 62, 1993, 62 :179-239
[26]  
PENG M, 1993, LEUKEMIA, V7, P104
[27]   Cytotoxic T lymphocyte responses to Epstein-Barr virus [J].
Rickinson, AB ;
Lee, SP ;
Steven, NM .
CURRENT OPINION IN IMMUNOLOGY, 1996, 8 (04) :492-497
[28]  
RICKINSON AB, 1982, CLIN EXP IMMUNOL, V50, P347
[29]   The X-linked lymphoproliferative-disease gene product SAP regulates signals induced through the co-receptor SLAM [J].
Sayos, J ;
Wu, C ;
Morra, M ;
Wang, N ;
Zhang, X ;
Allen, D ;
van Schaik, S ;
Notarangelo, L ;
Geha, R ;
Roncarolo, MG ;
Oettgen, H ;
De Vries, JE ;
Aversa, G ;
Terhorst, C .
NATURE, 1998, 395 (6701) :462-469
[30]   Recognition of B-CLL cells experimentally infected with EBV by autologous T lymphocytes [J].
Tomita, Y ;
Avila-Cariño, J ;
Yamamoto, K ;
Mellstedt, H ;
Klein, E .
IMMUNOLOGY LETTERS, 1998, 60 (2-3) :73-79