Paired epstein‐barr virus‐carrying lymphoma and lymphoblastoid cell lines Burkitt's lymphoma patients: Comparative sensitivity to non‐specific and to allo‐specific cytotoxic responses <i>in vitro</i>

Rooney, Cliona M.; Rickinson, Alan B.; Moss, Denis J.; Lenoir, Gilbert; Epstein, M. A.

doi:10.1002/ijc.2910340310

Cited by 51 publications

(28 citation statements)

References 40 publications

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“…This is not due to a general resistance to cell-mediated cytotoxicity. BL/LCL pairs derived from the same donor and kept in culture during similar periods were equally sensitive to natural and interferon-activated killer cells (20,32). This was also true for the cell lines used in the present study (data not shown).…”

Section: Discussionsupporting

confidence: 77%

See 1 more Smart Citation

Differentiation-dependent sensitivity of human B-cell-derived lines to major histocompatibility complex-restricted T-cell cytotoxicity.

Torsteinsdóttir¹,

Masucci²,

Ehlin‐Henriksson³

et al. 1986

Proc. Natl. Acad. Sci. U.S.A.

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Sets of Burkitt lymphoma lines and Epstein-Barr virus (EBV)-transformed lymphoblastoid cell lines (LCLs) derived from the same individuals were compared for sensitivity to cytotoxic T-lymphocyte (CTL) clones. Major histocompatibility complex class I antigen-restricted CTL clones were generated by stimulating the lymphocytes of an EBV-seropositive individual with the autologous LCL. One clone (BK-20) lysed the autologous and allogeneic HLA-Allexpressing LCLs but not mitogen-induced B lymphoblasts. Thus the clone was selectively cytotoxic for LCLs. Allospecific CTL clones directed against the HLA-All antigen were generated from an EBV-seronegative individual. One clone (WP-36) was selectively cytotoxic for the appropriate allospecific LCL, whereas another clone (WP-21) lysed also T and B lymphoblasts. None of the four Burkitt lymphoma lines established in parallel with the CTL-sensitive LCLs were lysed. Two of the Burkitt lymphoma lines were EBV-negative, and EBV-positive sublines were derived from these by in vitro infection. One but not the other of the two convertants became sensitive to all three types of CTL clones. The CTL-sensitive converted line had also acquired some LCL characteristics: increased cell size, aggregation, and a shift in several of the B-cell-specific surface markers. The CTL-resistant convertant expressed EBV antigens but showed no phenotypic change. These findings suggest that the cellular phenotype plays a decisive role in the sensitivity of B-cell-derived lines to the lytic effect of LCL-selective autologous and allogeneic CTLs.

show abstract

Section: Discussionsupporting

confidence: 77%

“…We have used "trios" composed of an in vitro-transformed LCL, an EBV-negative BL line, and an EBV-converted subline of the latter, derived from the same patient, and "duos" consisting of a LCL and an EBV-carrying BL (18)(19)(20). The CTL clones were generated by stimulation with autologous and allogeneic EBV-infected B cells.…”

mentioning

confidence: 99%

Differentiation-dependent sensitivity of human B-cell-derived lines to major histocompatibility complex-restricted T-cell cytotoxicity.

Torsteinsdóttir¹,

Masucci²,

Ehlin‐Henriksson³

et al. 1986

Proc. Natl. Acad. Sci. U.S.A.

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“…They are as sensitive to natural killer cells and to interferon-and mixed lymphocyte culture-activated nonspecific killer cells as were the corresponding LCLs (9,22). Moreover, as shown in Fig.…”

Section: Resultsmentioning

confidence: 85%

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

Masucci¹,

Torsteindottir²,

Colombani³

et al. 1987

Proc. Natl. Acad. Sci. U.S.A.

124

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Epstein-Barr virus (EBV)-carrying Burkitt lymphoma (BL) cells are relatively or completely resistant to the lytic effect of major histocompatibility complex class I HLA antigen-restricted cytotoxic T lymphocytes (CTLs) generated by stimulating lymphocytes of EBV-seropositive donors with the autologous EBV-transformed lymphoblastoid cell line (LCL). We previously found that EBV-negative and EBVcarrying BL lines derived from HLA-All-positive donors were not only resistant to lysis by the HLA-All-restricted CTL generated by stimulation with the autologous LCL, but also to HLA-All-specific CTL derived from lymphocytes of an EBVseronegative donor stimulated with an allogeneic LCL. Using the same and additional cell lines, we now show that the CTL resistance of the BL lines is probably due to a selective down-regulation of HLA-All. We also show that the EBVencoded latent membrane protein is expressed at a lower level in the EBV-carrying BL lines than in EBV-transformed LCLs. Only one of eight in vitro EBV-converted BL lines that shifted to a more LCL-like growth pattern expressed LMP at a high level. This line also reexpressed the HLA-All antigen that was undetectable in its EBV-negative progenitor. Our rmdings suggest that the typical BL cell phenotype is associated with low expression of both proteins.Reciprocal translocations juxtapose the cellular c-myc gene (MYC gene in humans) to an immunoglobulin locus in Epstein-Barr virus (EBV)-carrying and EBV-negative Burkitt lymphoma (BL) lines and in mouse and rat plasmacytomas (1, 2). It has been suggested that the translocations contribute to the tumorigenic process by bringing the c-myc gene under the regulatory influence of the adjacent, highly active immunoglobulin locus. This concept is supported by the high incidence of pre-B-cell and B-cell lymphomas in transgenic mice that carried immunoglobulin heavy chain Igh enhancer-myc constructs (3) and the appearance of translocation-free plasmacytomas in pristane oil-treated BALB/c mice infected with myc-expressing retroviral constructs (4). However, the monoclonality of the B-cell tumors that arose in the transgenic mice carrying the Igh enhancer-myc construct indicates that at least one additional step is needed for full tumorigenicity.EBV-carrying BL cells are relatively or completely resistant to the lytic effect of major histocompatibility complex (MHC) class I HLA antigen-restricted cytotoxic T lymphomas (CTLs) generated by stimulating lymphocytes of EBVseropositive donors with the autologous EBV-transformed lymphoblastoid cell line (LCL) (5,6). This was taken to suggest that escape from immune surveillance may play a role in the pathogenesis of the EBV-positive BL lines.We have found that EBV-negative and EBV-carrying BL lines derived from HLA-A1l-positive donors were not only resistant to lysis by the HLA-All-restricted CTLs generated by stimulation with the autologous LCL but also the HLAAll-specific CTLs generated by stimulating the lymphocytes of an EBV-seronegative donor with an allogeneic LCL (6). We ...

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“…IARC-BL18, BL72, BL74 and Elija are Burkitt's lymphoma cell lines (Rooney et al, 1984(Rooney et al, , 1985 kindly given by G.M.Lenoir and A.B.Rickinson. PRBL18 is a human lymphoblastoid cell line made by infecting peripheral lymphocytes from a seronegative English donor with EBV from BL18 (Rooney et al, 1984(Rooney et al, , 1985. Raji cells are derived from an African Burkitt's lymphoma (Pulvertaft, 1965).…”

Section: Methodsmentioning

confidence: 99%

A spliced Epstein-Barr virus gene expressed in immortalized lymphocytes is created by circularization of the linear viral genome.

1988

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Paired epstein‐barr virus‐carrying lymphoma and lymphoblastoid cell lines Burkitt's lymphoma patients: Comparative sensitivity to non‐specific and to allo‐specific cytotoxic responses in vitro

Cited by 51 publications

References 40 publications

Differentiation-dependent sensitivity of human B-cell-derived lines to major histocompatibility complex-restricted T-cell cytotoxicity.

Differentiation-dependent sensitivity of human B-cell-derived lines to major histocompatibility complex-restricted T-cell cytotoxicity.

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

A spliced Epstein-Barr virus gene expressed in immortalized lymphocytes is created by circularization of the linear viral genome.

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