Production and characterization of marmoset lymphoblastoid interferon

Abb, Jochen; Abb, Hannelore; Deinhardt, Friedrich

doi:10.1002/ijc.2910290113

Cited by 8 publications

(7 citation statements)

References 14 publications

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“…The hypothesis that tumor promoters can have contrasting effects on cells from different stages along the same pathway is also supported by data in this communication and by previous reports on the effect of TPA on T lymphocytes (39)(40)(41)(42)(43). In the present paper we showed that nanomolar concentrations of TPA can inhibit proliferation of these leukemic T lymphoblasts.…”

Section: Cellssupporting

confidence: 89%

“…In the present paper we showed that nanomolar concentrations of TPA can inhibit proliferation of these leukemic T lymphoblasts. This effect, however, is in contrast to the known comitogenic effect of TPA on more mature T lymphocytes, in which stimulation of proliferation by these cells was observed (39)(40)(41)(42)(43). Another effect of phorbol esters on MOLT-3 cells that is distinguishable from the effects on the other leukemic hemopoietic cells (20,(22)(23)(24) is that MOLT 3 cells do not become adhesive after treatment with TPA.…”

Section: Cellsmentioning

confidence: 90%

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Phorbol esters induce differentiation in human malignant T lymphoblasts

Nagasawa

Mak

1980

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

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At nanomolar concentrations, phorbol esters, a class of potent tumor promoters, can promote differentiation in the human malignant T-lymphoblastic cell line MOLT-3. The optimal dose for induction, as measured by the increase of the number of cells containing sheep erythrocyte receptors (E-rosette assay), is between 8 and 16 nM 12-OLtetradecanoylphorbol 13-acetate (TPA), although there were significant increases of E-rosette-positive (E+) cells at concentrations as low as 1.6 nM TPA. The induction was linear for 4 days, then it reached a plateau. This induction was independent of the cell densities of the cultures, and the viability of the E+ cells remained high (95-100%) even after 10 days of culture in the presence of the tumor promoters. The E+ cells, when measuredwith the more stable 2-aminoethylisothiouronium bromide E-rosette assay, indicated that virtually all (75-95%) of the MOLT-3 cells became E+ by 4 days in culture. This induction by TPA was also accompanied by a dramatic drop in the plating efficiencies and a reduction in DNA synthesis. Examination of phorbol and other phorbol esters indicated that the ability to induce these cells correlated well with the tumor-promoting activities of these compounds, because only TPA and to a lesser extent phorbol 12,13,-dibenzoate induced E+ cells, while phorbol and 4a-phorbol 12,13-didecanoate had no effect. Studies of MOLT-3 cells depleted of E+ cells indicated that the induction of E+ cells cannot be explained solely on the basis of enrichment or stimulation of the background E+ cells in MOLT-3 cultures. Finally, we have shown that TPA also affected another differentiation marker, the loss of the enzyme terminal deoxyribonucleotidyl transferase. Terminal transferase activities and percentages of terminal-transferase-positive cells in these cultures were reduced to as low as 1/10th in 4 days in the presence of 16 nM TPA.

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Section: Cellssupporting

confidence: 89%

Section: Cellsmentioning

confidence: 90%

Phorbol esters induce differentiation in human malignant T lymphoblasts

Nagasawa

Mak

1980

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

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“…Pretreatment ofthe CEM or CEM-CL3 cells with PMA made these cells less susceptible to mitomycin C inhibition of [3H]thymidine incorporation than cells that had not been treated with PMA. Furthermore, as described (22,23), treatment of PBLs with PMA not only does not suppress [3H]thymidine incorporation but rather stimulates it.…”

Section: Resultsmentioning

confidence: 70%

Differentiation of human T-lymphoid leukemia cells into cells that have a suppressor phenotype is induced by phorbol 12-myristate 13-acetate.

Ryffel¹,

Henning²,

Huberman³

1982

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

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Treatment of cultured human T-lymphoid (CEM) leukemia cells with nanomolar concentrations ofphorbol 12-myristate 13-acetate (PMA) resulted in a reduction in cell growth and in the acquisition of a surface antigenic pattern that is common to both suppressor and cytotoxic T lymphocytes. This antigenic pattern was detected by OKT Phorbol 12-myristate 13-acetate (PMA) and related phorbol diesters promote tumor formation in mouse skin (1, 2). A number of cellular events, including alterations in differentiation processes, have been attributed to the action of these agents (3). In some human melanoma cells (4) and in myeloid (5-7) and lymphoid leukemia cells (8-10), these agents can induce differentiation markers. In the T-lymphoid leukemia cells, phorbol esters were reported to increase the fraction of cells with receptors for sheep erythrocytes, reduce the level of terminal deoxynucleotidyltransferase activity, and alter cell morphology (9, 10). Changes in these markers, however, are not sufficient to characterize a specific differentiated state-e.g., differentiation into cells with suppressor, cytotoxic, inducer, or helper functions. Recently, Reinherz et aL (11) showed that the antigenic pattern, of immature human T lymphocytes changes during the maturation process in the thymus. Thus, discrete stages of human T-cell differentiation can be analyzed in normal and leukemia cells, by monoclonal antibodies directed against stagespecific surface antigens (12)(13)(14).We report here that tumor-promoting phorbol diesters can induce differentiation of a human T-lymphoid leukemia cell (CEM) into a cell type with an antigenic pattern and functional property that resembles a mature suppressor T lymphocyte.

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“…We therefore wished to examine whether PKC activation in T cells has a role in regulating expression of the TCR a and pchain genes. To address this question, we used tumor-promoting phorbol esters (PE), which can: (a) mimic the effects of [I 60161 DG by activating PKC (6), (b) trigger T cell activation [5, [8][9][10][11] and (c) down-regulate and phosphorylate the TCRassociated T3 complex [12]. We show here that PKC-activating PE augment expression of the TCR P-chain gene in the murine EL4 thymoma line, and that this effect is independent from activation of the IL 2 gene.…”

Section: Introductionmentioning

confidence: 99%

Protein kinase C‐activating phorbol esters augment expression of T cell receptor genes

1987

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Tumor-promoting phorbol esters (PE) can modulate cellular functions and cell surface determinant expression in a variety of cell types, including T lymphocytes, presumably by activating the enzyme, protein kinase C (PKC). To examine whether PKC might be involved in regulating the expression of genes encoding the antigen-specific T cell receptor (TCR), we cultured the murine thymoma line, EL4, in the presence of 12-O-tetradecanoylphorbol 13-acetate (TPA) and analyzed the expression of TCR alpha or beta-chain genes by Northern blots. TPA stimulation of an interleukin 2 (IL 2)-producing variant, EL4+, induced a 3-4-fold increase in TCR beta, but not alpha, chain mRNA. Maximal increase was obtained with 3 ng/ml TPA and 12 h of stimulation. This effect appeared related to PKC activation because other tumor-promoting PE known to be PKC activators, but not inactive PE, induced the same increase. TPA stimulation of EL4+ cells also induced de novo expression of the IL 2 gene and subsequent secretion of this lymphokine. However, the increased expression of the TCR beta-chain gene and the induction of the IL 2 gene were not linked since expression of TCR beta-chain mRNA was increased to a similar degree in EL4+ and IL 2-nonproducing EL4- sublines, and cyclosporin A selectively blocked TPA-induced IL 2-gene expression in EL4+ cells without affecting the increase in TCR beta-chain mRNA. These findings suggest that PKC activation, an event that supposedly occurs after antigen-mediated triggering of the TCR, can regulate the expression of at least some of the genes encoding this receptor.

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Production and characterization of marmoset lymphoblastoid interferon

Cited by 8 publications

References 14 publications

Phorbol esters induce differentiation in human malignant T lymphoblasts

Phorbol esters induce differentiation in human malignant T lymphoblasts

Differentiation of human T-lymphoid leukemia cells into cells that have a suppressor phenotype is induced by phorbol 12-myristate 13-acetate.

Protein kinase C‐activating phorbol esters augment expression of T cell receptor genes

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