The intravenous administration of syngeneic spleen cells (SPCs) briefly pulsed with antigen in vitro, results in a profound state of IgE antibody unresponsiveness. In Balb/c mice, the primary response of anti-DNP, anti-beef insulin and anti-ovalbumin IgE antibody is completely suppressed by the administration of antigen-pulsed spleen cells, 1 × 107, 5 × 107 and 1 × 108, respectively. This suppression is antigen specific and effects both primary and secondary immune responses. Furthermore, the immune response to dinitrophenylated Keyhole limpet hemocyanin (DNP-KLH) is most extensively suppressed by DNP-KLH pulsed SPCs, intermediately suppressed by KLH-pulsed SPCs and minimally suppressed by dinitrophenylated mouse gamma globulin or dinitrophenylated mouse serum albumin pulsed SPCs. Suppressing directly cells specific for hapten and carrier, hapten carrier protein pulsed SPCs would caused the additive suppressive effect. The suppression is induced strongly by the intravenous administration of antigen pulsed spleen cells, slightly by the subcutaneous administration and is not induced by the intravenous administration of antigen solution in phosphate buffer saline. This suppression may be mediated by either of two different mechanisms: one of them is responsible for the immediate tolerance which is induced without any suppressor cells 1 day after the administration of antigen pulsed SPCs, and the other is responsible for the suppression transferred by suppressor cells or factors to normal mice 7 days after the administration of antigen pulsed SPCs. This method in which IgE antibody response is suppressed by the administration of cells briefly pulsed in vitro with antigen, provides a powerful tool to analyze the first step of antigen specific suppression developed in vivo by conventional antigens.
SUMMARY.Membrane-bound cation stimulated adenosine-triphosphatase is thought to be closely associated with active ion transport phenomena. As this enzyme system requires the combination of both sodium and potassium ions for full activation its mechanism of action has been investigated under these conditions. Using adenosine triphosphate labelled with P^ô nly in the terminal position as substrate for the reaction we have been able to show that ATP^2 is hydroiysed to adenosine diphosphate and radioactive orthophosphate via a phosphorylated intermediate. Sodium but not potassium ions are required for the formation of this intermediate and adenosine diphosphate; potassium ions are subsequently required for dephosphorylation of the intermediate complex with tlie release of P-''^ orthophosphate -that is, both sodium and potassium ions arc required for the turnover of the intermediate in a two step reaction.The cardiac glycoside ouabain (Strophanthin-G) is without effect upon the formation of this intermediate complex, but can completely inhibit the K+ -requiring dephosphorylation reaction. Preliminary experiments indicate that sodium ions are bound to the enzyme system during the phosphorylation reaction and are released when this complex is broken down. Solvent extraction procedures designed to remove phospholipid components did not decrease the specific activity of the phosphorylaled intenncdiate which suggests that it is phosphoprotein in nature.
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