Cyclic AMP Changes as a Consequence of Tumor-Normal Cell Interactions

Abstract

Our present concentration on the role of cAMP-mediated events in immune responses is the direct consequence of our earlier discovery and analysis of the effects of nucleic acid breakdown products on population changes in bacteria and on antibody formation (1,2). Critical turning points in establishing a basis for the stimulatory activity of DNA breakdown products were: first, the discovery that double-stranded synthetic polynucleotides, including poly A:U, poly G:C, and poly I:C, were even better and more consistent stimulators than the natural nucleic acids previously employed, and second, the discovery of cAMP and its role in regulating cell function. In these studies of ours, the polynucleotide of choice was poly A:U, because it is neither pyrogenic nor toxic compared to poly I:C.