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Target-Effector Interaction in the Natural Killer Cell System

IV. Modulation by Cyclic Nucleotides

John C. Roder and Margareta Klein
J Immunol December 1, 1979, 123 (6) 2785-2790;
John C. Roder
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Margareta Klein
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Abstract

Dibutyryl cAMP (dB-cAMP) and the cAMP elevating agents, prostaglandin E1, theophylline, and histamine markedly suppressed NK cytolytic function in a dose-and rate-dependent manner. The inhibition was rapidly induced and persisted in the presence of the drugs. Separate pretreatment of targets and highly purified NK cells, isolated by a target binding and velocity sedimentation technique, revealed that PGE1 and dB-cAMP acted at the level of the effector cell in a short-term cytolytic assay. In contrast to the inhibitory effects of cAMP elevating agents, dB-cGMP and carbamylcholine caused a small but significant acceleration in the rate of lysis and could compete with inhibitory doses of dB-cAMP to reduce the level of suppression thereby suggesting that the cAMP-cGMP ratio might be important in NK-mediated lysis. Insulin had no effect on NK activity, whereas T cell-mediated cytolysis was augmented by insulin and cGMP if the effector cells were taken early after alloimmunization but not later. Neither cAMP- nor cGMP-elevating agents affected the frequency of NK-target cell conjugates. These results are compatible with the hypothesis that cyclic nucleotides may be involved in triggering the lytic event within NK cells.

Footnotes

  • ↵1 This work was supported by the Killam program of the Canada Council and National Cancer Institute Contract NO1 CB 64023.

  • Received January 8, 1979.
  • Accepted September 12, 1979.
  • Copyright © 1979 by The American Association of Immunologists, Inc.

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The Journal of Immunology
Vol. 123, Issue 6
1 Dec 1979
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Target-Effector Interaction in the Natural Killer Cell System
John C. Roder, Margareta Klein
The Journal of Immunology December 1, 1979, 123 (6) 2785-2790;

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Target-Effector Interaction in the Natural Killer Cell System
John C. Roder, Margareta Klein
The Journal of Immunology December 1, 1979, 123 (6) 2785-2790;
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