Literature DB >> 6090321

Paired Epstein-Barr virus-carrying lymphoma and lymphoblastoid cell lines from Burkitt's lymphoma patients: comparative sensitivity to non-specific and to allo-specific cytotoxic responses in vitro.

C M Rooney, A B Rickinson, D J Moss, G M Lenoir, M A Epstein.   

Abstract

Paired Epstein-Barr (EB) virus-carrying cell lines have been established from Burkitt's lymphoma (BL) patients; one the BL-cell line derived from the malignant cells of the tumour and bearing the relevant chromosomal translocation, the other the diploid lymphoblastoid cell line (LCL) derived from the patient's normal B cells by experimental infection with the virus. Comparative studies have shown that both BL and LCL cells are relatively resistant to fresh NK cells but are more susceptible to in vitro-activated NK cells; individual pairs differ as to whether the BL or LCL cells are more sensitive to such effectors. With most cell pairs studied, the two cell types were equally efficient at inducing NK-cell activation in vitro. When the in vitro stimulation protocol was changed to favour the induction of allo-specific responses, most BL cells were noticeably poorer stimulators than the corresponding LCL although both cell types induced a similar pattern of cytotoxicity; this appeared to be directed against HLA class I allo-antigens and could be inhibited by class I antigen-specific monoclonal antibodies. Most BL target lines, though susceptible to this allo-specific lysis, were significantly less so than the corresponding LCL However, only 1/7 BL-cell lines tested vis-à-vis the LCL gave evidence of a gross reduction in HLA antigen expression and this was immediately apparent from both serological typing and cellular analysis.

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Year:  1984        PMID: 6090321     DOI: 10.1002/ijc.2910340310

Source DB:  PubMed          Journal:  Int J Cancer        ISSN: 0020-7136            Impact factor:   7.396


  19 in total

1.  Epstein-Barr virus and the somatic hypermutation of immunoglobulin genes in Burkitt's lymphoma cells.

Authors:  R S Harris; D S Croom-Carter; A B Rickinson; M S Neuberger
Journal:  J Virol       Date:  2001-11       Impact factor: 5.103

2.  Defective generation of killer cells against spontaneously Epstein-Barr virus (EBV)-transformed autologous B cells in a fatal EBV infection.

Authors:  M Yanagisawa; M Kato; K Ikeno; T Kobayashi; Y Miyagawa; A Komiyama; T Akabane
Journal:  Clin Exp Immunol       Date:  1987-05       Impact factor: 4.330

3.  Identification of type B-specific and cross-reactive cytotoxic T-lymphocyte responses to Epstein-Barr virus.

Authors:  B M Kerr; N Kienzle; J M Burrows; S Cross; S L Silins; M Buck; E M Benson; B Coupar; D J Moss; T B Sculley
Journal:  J Virol       Date:  1996-12       Impact factor: 5.103

4.  Two families of sequences in the small RNA-encoding region of Epstein-Barr virus (EBV) correlate with EBV types A and B.

Authors:  J R Arrand; L S Young; J D Tugwood
Journal:  J Virol       Date:  1989-02       Impact factor: 5.103

5.  Down-regulation of class I HLA antigens and of the Epstein-Barr virus-encoded latent membrane protein in Burkitt lymphoma lines.

Authors:  M G Masucci; S Torsteindottir; J Colombani; C Brautbar; E Klein; G Klein
Journal:  Proc Natl Acad Sci U S A       Date:  1987-07       Impact factor: 11.205

6.  Influence of the Epstein-Barr virus nuclear antigen EBNA 2 on the growth phenotype of virus-transformed B cells.

Authors:  A B Rickinson; L S Young; M Rowe
Journal:  J Virol       Date:  1987-05       Impact factor: 5.103

7.  A promoter for the highly spliced EBNA family of RNAs of Epstein-Barr virus.

Authors:  M Bodescot; M Perricaudet; P J Farrell
Journal:  J Virol       Date:  1987-11       Impact factor: 5.103

8.  A family study of the X-linked lymphoproliferative syndrome: evidence for a B cell defect contributing to the immunodeficiency.

Authors:  I Ando; G Morgan; R J Levinsky; D H Crawford
Journal:  Clin Exp Immunol       Date:  1986-02       Impact factor: 4.330

9.  Epstein-Barr virus latent messages with shuffled leader exons: remnants of circumgenomic transcription?

Authors:  L Qu; D T Rowe
Journal:  J Virol       Date:  1995-02       Impact factor: 5.103

10.  Tumor indoleamine 2,3-dioxygenase (IDO) inhibits CD19-CAR T cells and is downregulated by lymphodepleting drugs.

Authors:  Soranobu Ninomiya; Neeharika Narala; Leslie Huye; Shigeki Yagyu; Barbara Savoldo; Gianpietro Dotti; Helen E Heslop; Malcolm K Brenner; Cliona M Rooney; Carlos A Ramos
Journal:  Blood       Date:  2015-05-04       Impact factor: 22.113

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