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J Pharm Sci. 1989 Jan;78(1):8-10.

Potential use of an antagonist of cAMP-dependent protein kinase to block inhibition and modulate T-cell receptor-triggered activation of cytotoxic T-lymphocytes.

Author information

1
Laboratory of Immunology, National Institutes of Health, Bethesda, MD 20892.

Abstract

It was recently established that cAMP-dependent protein kinase (PK-A) inhibits both early and late stages of T-cell receptor-mediated cytotoxic T-lymphocyte (CTL) activation. We suggested that PK-A may function as a part of a biochemical down-regulating "off" signal in regulation of CTL activities. It is proposed here to use antagonists of PK-A to block such an inhibitory pathway, thereby enhancing immune response. We explored this possibility using the diastereomer of adenosine cyclic 3',5'-phosphorothioate (Rp-cAMPS), a recently described PK-A antagonist. It is shown that Rp-cAMPS blocks cAMP-induced inhibition of lytic activity and of exocytosis of granules from CTL. The immunomodulating potential of cAMP analogues which inhibit PK-A is discussed.

PMID:
2785178
DOI:
10.1002/jps.2600780104
[Indexed for MEDLINE]

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