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M Stoeck

Publications and source records attributed to M Stoeck.

25 records · Page 2Linked to original sources
PubMed1988

Induction of responsiveness to IL 2 in Con A-stimulated rat lymphoid cells requires synergistic action of IL 1 and the accessory cell membrane.

Rat spleen or lymph node cells stimulated with Con A and cultured at a low density of 1 x 10(5) cells per ml proliferated in response to IL 2-containing supernatants and thus expressed receptors for IL 2. Cells depleted of accessory cells either by passage over a glassbead-column or by treatment with the lysosomotropic agent leucine methyl ester (Leu-OMe) did not proliferate in response to IL 2-containing supernatants. The diminished proliferative response after adherent cell depletion could be reconstituted by the addition of peritoneal exudate cells (PEC). Reconstitution could also be achieved by synergistic action of IL 1 and paraformaldehyde-fixed peritoneal exudate cells, indicating an important role for the accessory cell membrane in the induction of IL 2-mediated proliferation.

Animals↗
PubMed1987

Induction of responsiveness to interleukin 2 in mouse lymphocytes by synergistic action of ionophore A 23187 and diacylglycerol.

We investigated whether the protein kinase C-binding agents 12-O-tetradecanoyl-phorbol-13-acetate (TPA) and 1-oleoyl-2-acetyl-rac-glycerol (OAG) induced reactivity to interleukin 2 (IL-2) in mouse lymphocytes. 10(-8) M TPA was a strong inducer of reactivity to IL-2 measured by [3H]thymidine incorporation. In contrast OAG alone (6-25 micrograms/ml) did not induce a significant IL-2 mediated proliferative response. Cells stimulated with the ionophore A 23187 + OAG neither proliferated nor produced IL-2. In contrast, cells stimulated with A 23187 + OAG + IL-2 showed a significant proliferative response, indicating the expression of functional high affinity IL-2 receptors. The expression of reactivity to IL-2 induced by A 23187 + OAG was inhibited by 0.04 mM Mn2+; in contrast the TPA-mediated induction of IL-2 responsiveness was not affected by Mn2+. The data suggest differences in the mechanism of induction of IL-2 responsiveness by the two protein kinase C-binding agents, TPA and OAG.

Animals↗
PubMed1985

Studies on the mechanism whereby cyclosporin A inhibits T-lymphocyte activation.

The immunosuppressive drug Cyclosporin A (CyA) inhibited the ConA-induced DNA synthesis in C57B1/6 spleen cells at a concentration of 40 ng/ml totally; this inhibition could not be overcome by the addition of highly purified interleukin-1. ConA-induced RNA synthesis was also inhibited by concentrations of 40 or 200 ng/ml CyA, although total inhibition could not be achieved. In contrast, lipopolysaccharide-induced proliferation could not be inhibited. CyA at a concentration of 40 ng/ml also inhibited the ConA-induced production of interleukin-2 by mouse spleen cells, this inhibition was not due to a toxic mechanism. On the contrary, the proliferative response of T cell blasts from a long-term T cell line (M2) to interleukin-2 containing supernatants was not inhibited by concentrations of 40 or 200 ng/ml CyA; only at 20-100-fold higher concentrations partial inhibition could be observed. One of the earliest events in the course of lymphocyte activation, the enhanced incorporation of unsaturated fatty acids into the lymphocyte plasma membranes; was also inhibited by concentrations of CyA, which abrogated the ConA-induced DNA synthesis. The inhibition of the enhanced incorporation of 14C-oleic acid and 14C-linoleic acid, which are incorporated by the membrane-bound lysolecithin-acyltransferase, thus suggests a molecular site of action for CyA.

Animals↗
PubMed1983

Inhibition of mitogen-induced lymphocyte proliferation by ouabain: interference with interleukin 2 production and interleukin 2 action.

Since the discovery of IL 2 it has been possible to dissect the mitogenic activation of T lymphocytes into two steps: first, the production of IL 2; and second, the response of IL 2-dependent T cell blasts to IL 2. We investigated the influence of ouabain, a known inhibitor of T cell activation, on the production of and the response to IL 2 in mouse T lymphocytes. Ouabain dose-dependently inhibited DNA synthesis in Con A activated C57BL/6 spleen cells; inhibition below background levels occurred at a concentration of 5 X 10(-4) mol/liter. The action of IL 2 was assayed on a mouse T cell line, named M 2, derived from C57BL/6 spleen cells and maintained in continuous IL 2-dependent culture for more than 21 mo. Ouabain dose-dependently inhibited the response of these cells to mouse IL 2 with optimal inhibition at 10(-3) mol/liter ouabain. The production of IL 2 by Con A-stimulated C57BL/6 spleen cells was also totally inhibited by 10(-3) mol/liter ouabain; 10(-4) mol/liter ouabain inhibited IL 2 production partially, and 10(-5) mol/liter and 10(-6) mol/liter ouabain had no inhibitory effect. The ouabain-mediated inhibition of IL 2 production and of IL 2 action was not due to a nonspecific toxicity, because the preincubation of spleen cells with 10(-3) mol/liter ouabain for 24 hr did not impair their ability to produce IL 2, nor was the response of M 2 cells to exogenously added IL 2 abrogated by the preincubation of the cells with 10(-3) mol/liter ouabain. The data suggest that ouabain acts on two steps during the induction of T cell activation.

Animals↗
PubMed1982

The effect of phorbol-myristate acetate and concanavalin A on the growth of interleukin-2-dependent T-cell lines.

We tested the effect of phorbol myristate acetate (PMA) and of Con A on the growth of two Il-2 dependent T cell-lines. Il-2 dependent growth, as measured by 3H-TDR incorporation or viable cell counts was enhanced by PMA (5-100 ng/ml) and inhibited by Con A. These effects were only reproducible in the presence of intermediate concentrations of Il-2 containing supernatant. The enhancing effect of PMA was probably due to a positive influence on the replication rate since the drug had no visible effect on cell survival and since no evidence was found for the induction of Il-2 production by the cell-lines.

Animals↗