Absence, or low expression, of leukocyte adhesion molecules CDI1 and CD18 on burkjtt lymphoma cells

Patarroyo, Manuel Elkín; Prieto, J. Prieto; Ernberg, Ingemar; Gahmberg, Carl G.

doi:10.1002/ijc.2910410623

Cited by 56 publications

(16 citation statements)

References 44 publications

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“…We found that the level of expression of class-I MHC antigens detected using the W6i32 MAb, which recognizes a monomorphic HLA A, B, C determinant, was significantly lower (p < 0.05) in Burkitt cells with t(8;14) than in lymphoblastoid cells. Decreased expression of class-I MHC antigens has also been reported recently in other Burkitt cells using the same antibody W6/32 (Patarroyo et al, 1988) and a panel of MAbs directed against several polymorphic HLA class-I determinants (Torsteinsdottir et al, 1988), although previous reports indicated that there was no difference in class-I MHC antigen expression between other Burkitt and lymphoblastoid cell lines using the W6/32 MAb (Rooney et al, 1984Masucci et al, 1987). We also found a significant correlation (r = 0.70, p < 0.05) between the expression of insulin receptors and class-I MHC antigens when data for both lymphoblastoid and Burkitt cells were combined (Fig.…”

Section: Discussionmentioning

confidence: 64%

Insulin receptor expression in burkitt lymphoma cell lines

Newman

Harrison

1989

Intl Journal of Cancer

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The specific binding of insulin to 7 different Burkitt lymphoma cell lines containing chromosomal translocations t(8;14), t(8;2) and t(8;22) was markedly decreased when compared to binding to lymphoblastoid cells of normal karyotype derived from Burkitt lymphoma patients or the human IM-9 lymphoblastoid line. The number of insulin-binding sites on intact Burkitt cells was decreased by greater than 90% compared to lymphoblastoid cells, with no change in affinity. This decrease in binding was paralleled by reduced amounts of insulin receptor alpha (Mr 130,000) and beta (Mr 95,000) subunits detected by cell-surface-labelling and insulin receptor mRNA transcripts, indicating that transcription of receptor mRNA is decreased in Burkitt cells compared to lymphoblastoid cells and/or that receptor mRNA is less stable. Burkitt cells displayed negligible insulin-stimulated beta subunit auto-phosphorylation, which could reflect either their decreased number of receptors or a defect in signal transduction. Structural analysis also revealed that the Burkitt cells had an increase in a precursor form (Mr 210,000) of the receptor, suggesting that decreased expression of the receptor may be associated with defective processing. Four Burkitt cell lines with t(8;14) also had reductions of 45-100% in expression of class-1 major histocompatibility (MHC) antigens. The expression of insulin receptors in both Burkitt and lymphoblastoid cells correlated with the expression of class-1 MHC antigens. There was also an inverse correlation between the expression of c-myc and both insulin receptors and class-1 MHC antigens. As the insulin receptor is absent on resting B cells and is induced after cell activation, the decrease in receptor expression on Burkitt cells may reflect their less activated phenotype compared to lymphoblastoid cells.

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Section: Discussionmentioning

confidence: 64%

Insulin receptor expression in burkitt lymphoma cell lines

Newman

Harrison

1989

Intl Journal of Cancer

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“…MW markers as in Figure 2. expression is also seen in Burkitt's lymphomas (Patarroyo et al, 1988). CD23, a B-cell-activation antigen, usually expressed by LCL but not BL , was also demonstrated on most of the monkey lymphomas.…”

Section: Discussionmentioning

confidence: 92%

Expression of epstein‐barr‐virus‐related nuclear antigens and B‐cell markers in lymphomas of SIV‐immunosuppressed monkeys

Feichtinger

Kaaya

et al. 1993

Intl Journal of Cancer

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Simian-immunodeficiency-virus(SIV)-infected cynomolgus monkeys develop B-cell lymphomas in approximately one third of the cases. We have now studied the expression of cynomolgus-Epstein-Barr-virus(cyno-EBV) nuclear antigens in 13 cyno-EBV-carrying SIVsm-associated monkey lymphomas and established cell lines from 3 of these tumors. Immunoblots of cell lysates were probed with polyspecific and monospecific reagents directed against human EB-virus EBNAI-6, and against the membrane protein LMPI. An EBNA2-cross-reacting protein was demonstrated in 8 lymphoma tissues (8/13) and in the 3 cell lines derived from the tumors. All tumors expressed a polypeptide with 50 to 55 kDa molecular weight, which cross-reacted with some antibodies to EBNAI. Absorption experiments with normal monkey tissue showed that this polypeptide was specific for the cyno-EBV-carrying lymphoma cells. Equivalents of EBNA3-6 and LMPI could not be detected. Immunophenotypical characterization showed that the monkey lymphomas were similar to human HIV-associated B-cell lymphomas. Malignant B-cell lymphomas in experimentally SIVsm-infected cynomolgus monkeys can be a model for EBV-associated lymphomagenesis in immunodeficiency states.

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“…In view of the evidence that lymphoblastoid cell lines expressing high levels of IL-6 are more tumorigenic than control lines, it was of interest to know whether these lines might display a w Burkitt's lymphoma-like phenotype (37)(38)(39)(40)(41)(42)(43). However, all :25,6M lymphoblastoid cell lines, regardless of how much IL-6 they nt produced and how tumorigenic they were, expressed similar levels of the B cell activation antigen CD23, and the cell adhe- Given that IL-6 promotes the proliferation ofEBV-immortalized cells (16)(17)(18), the tumorigenic effect of IL-6 could depend upon IL-6 providing a growth advantage to EBV-immor- tch Ed much of this bioactivity derived from murine IL-6 in the culture supernatant, because it was largely neutralized by a heteroantiserum to mouse IL-6 (28) and only to a small degree by a MAb to human IL-6 (29).…”

Section: Resultsmentioning

confidence: 99%

Impairment of natural killer functions by interleukin 6 increases lymphoblastoid cell tumorigenicity in athymic mice.

Tanner

Tosato²

1991

J. Clin. Invest.

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Expression of the human IL-6 gene in EBV-immortalized normal human B lymphocytes following retroviral-mediated transduction rendered these cells highly tumorigenic in athymic mice. The tumors were lymphomas composed of the originally inoculated human lymphoblastoid cells. Co-injection of IL-6 expressing EBV-immortalized cells with IL-6 nonexpressing control cells resulted in increased tumorigenicity of the IL-6 nonexpressing cells. The lymphoblastoid cells expressing IL-6 were indistinguishable from parental cell lines in morphology and in a variety of cell surface characteristics, and did not exhibit growth advantage over parental cell lines in vitro, such that increased tumorigenicity is unlikely to depend upon a direct oncogenic effect of IL-6 on the B cells. Rather, at high concentrations, IL-6 markedly inhibits human lymphoblastoid cell killing by IL-2-activated murine splenocytes in vitro, suggesting that IL-6-related tumorigenicity might depend upon IL-6 inhibiting cytotoxicity at the tumor site. Thus, production of IL-6 by tumor cells that results in natural killer cell dysfunctions illustrates a novel mechanism of tumor cell escape from immune surveillance. (J. Clin. Invest. 1991. 88:239-247.)

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Absence, or low expression, of leukocyte adhesion molecules CDI1 and CD18 on burkjtt lymphoma cells

Cited by 56 publications

References 44 publications

Insulin receptor expression in burkitt lymphoma cell lines

Insulin receptor expression in burkitt lymphoma cell lines

Expression of epstein‐barr‐virus‐related nuclear antigens and B‐cell markers in lymphomas of SIV‐immunosuppressed monkeys

Impairment of natural killer functions by interleukin 6 increases lymphoblastoid cell tumorigenicity in athymic mice.

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