Epstein-Barr virus (EBV) induces expression of B-cell activation markers on in vitro infection of EBV-negative B-lymphoma cells.

Calender, A ; Billaud, M ; et al.

In: Proceedings of the National Academy of Sciences of the United States of America, Jg. 84 (1987-11-01), Heft 22, S. 8060-4

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A set of B-cell activation markers, including the EBV/C3d receptor [complement receptor type 2 (CR2) (CD21)], the 45-kDa lymphoblastoid cell-associated (Blast-2) antigen (CD23), and the B-cell restricted activation (Bac-1) antigen (which was recently identified as a potential B-cell growth factor receptor) can be turned on by infecting lymphoma cells that are genome negative for Epstein-Barr virus (EBV) with the B95-8 immortalizing strain of the virus. The nonimmortalizing EBV variant, strain P3HR-1, which possesses a deletion within the BamHI WYH region of the genome containing the coding sequence for the EBV-determined nuclear antigen 2, does not induce expression of these markers. Other lymphoblastoid cell-associated antigen markers can be activated by infection with either immortalizing or nonimmortalizing viruses. These results suggest that the immortalizing potential of EBV is correlated with its ability to induce expression of B-cell activation markers, which are suspected to play a major role in the physiological pathway leading to lymphoid cell proliferation. The viral genomic region deleted in the nonimmortalizing strain of EBV seems to be required for activation of some of these markers. Human lymphoma cell lines, such as those used in this study, can thus help identify the specific EBV genes involved in lymphoid B-cell proliferation and the mechanism of action of these genes.

Titel:	Epstein-Barr virus (EBV) induces expression of B-cell activation markers on in vitro infection of EBV-negative B-lymphoma cells.
Autor/in / Beteiligte Person:	Calender, A ; Billaud, M ; Aubry, JP ; Banchereau, J ; Vuillaume, M ; Lenoir, GM
Link:	Full Text Finder (Volltext) E-Journal im Bestand der UB Hagen?
Zeitschrift:	Proceedings of the National Academy of Sciences of the United States of America, Jg. 84 (1987-11-01), Heft 22, S. 8060-4
Veröffentlichung:	Washington, DC : National Academy of Sciences, 1987
Medientyp:	academicJournal
ISSN:	0027-8424 (print)
DOI:	10.1073/pnas.84.22.8060
Schlagwort:	Cell Division Gene Expression Regulation Herpesvirus 4, Human genetics Humans Lymphocyte Activation Receptors, Complement 3d Tumor Cells, Cultured analysis Antigens, Neoplasm biosynthesis Antigens, Surface biosynthesis B-Lymphocytes analysis Burkitt Lymphoma pathology Cell Transformation, Viral Herpesvirus 4, Human physiology Receptors, Complement biosynthesis
Sonstiges:	Nachgewiesen in: MEDLINE Sprachen: English Publication Type: Journal Article; Research Support, Non-U.S. Gov't Language: English [Proc Natl Acad Sci U S A] 1987 Nov; Vol. 84 (22), pp. 8060-4. MeSH Terms: Cell Transformation, Viral* ; Antigens, Neoplasm / biosynthesis ; Antigens, Surface / biosynthesis ; B-Lymphocytes / analysis ; Burkitt Lymphoma / pathology ; Herpesvirus 4, Human / physiology ; Receptors, Complement / biosynthesis ; Cell Division ; Gene Expression Regulation ; Herpesvirus 4, Human / genetics ; Humans ; Lymphocyte Activation ; Receptors, Complement 3d ; Tumor Cells, Cultured / analysis References: Science. 1967 Sep 1;157(3792):1064-5. (PMID: 6036237) ; EMBO J. 1987 Jun;6(6):1637-42. (PMID: 3038527) ; J Gen Virol. 1973 Sep;20(3):391-4. (PMID: 4355332) ; Int J Cancer. 1973 May;11(3):499-520. (PMID: 4133943) ; Proc Natl Acad Sci U S A. 1974 Aug;71(8):3283-6. (PMID: 4369887) ; Nature. 1978 Apr 13;272(5654):629-31. (PMID: 205793) ; Int J Cancer. 1979 Feb;23(2):197-200. (PMID: 216641) ; Nature. 1980 Feb 7;283(5747):583-5. (PMID: 6928257) ; Int J Cancer. 1982 Apr 15;29(4):373-81. (PMID: 6282762) ; J Virol. 1982 Sep;43(3):952-68. (PMID: 6292473) ; J Virol. 1982 Sep;43(3):979-86. (PMID: 6292475) ; J Immunol. 1983 Apr;130(4):1985-9. (PMID: 6300235) ; Adv Cancer Res. 1982;37:319-80. (PMID: 6305160) ; Cancer Res. 1983 Oct;43(10):4562-8. (PMID: 6309371) ; J Immunol. 1983 Oct;131(4):1754-61. (PMID: 6413577) ; Hematol Oncol. 1983 Jan-Mar;1(1):21-9. (PMID: 6677560) ; Proc Natl Acad Sci U S A. 1984 Jul;81(14):4510-4. (PMID: 6087328) ; Proc Natl Acad Sci U S A. 1984 Dec;81(23):7632-6. (PMID: 6209719) ; Eur J Immunol. 1985 Jan;15(1):73-6. (PMID: 3155687) ; Int J Cancer. 1985 Feb 15;35(2):251-6. (PMID: 2982745) ; Proc Natl Acad Sci U S A. 1985 Mar;82(5):1490-3. (PMID: 2983347) ; J Immunol. 1985 May;134(5):3007-12. (PMID: 2984280) ; J Exp Med. 1985 Jul 1;162(1):45-59. (PMID: 2989413) ; Nature. 1985 Sep 19-25;317(6034):264-7. (PMID: 3876511) ; J Immunol Methods. 1985 Dec 17;85(1):65-74. (PMID: 3908562) ; Nature. 1986 Jan 16-22;319(6050):238-40. (PMID: 3003578) ; J Immunol. 1986 Mar 1;136(5):1745-51. (PMID: 3081632) ; J Virol. 1986 May;58(2):709-12. (PMID: 2422399) ; J Immunol. 1986 Aug 15;137(4):1208-13. (PMID: 3090143) ; Eur J Immunol. 1986 Sep;16(9):1075-80. (PMID: 2428624) ; J Exp Med. 1986 Nov 1;164(5):1455-69. (PMID: 2945890) ; EMBO J. 1986 Oct;5(10):2599-607. (PMID: 3023050) ; Proc Natl Acad Sci U S A. 1972 Feb;69(2):383-7. (PMID: 4333982) Substance Nomenclature: 0 (Antigens, Neoplasm) ; 0 (Antigens, Surface) ; 0 (Receptors, Complement) ; 0 (Receptors, Complement 3d) Entry Date(s): Date Created: 19871101 Date Completed: 19871223 Latest Revision: 20190501 Update Code: 20240513 PubMed Central ID: PMC299477

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