Alterations in beta-adrenoceptor density on T-lymphocytes upon activation with interleukin-2 and phytohaemagglutinin.

Cultivation of human peripheral blood T-lymphocytes in the presence of interleukin-2 (IL-2) and phytohaemagglutinin (PHA) caused biphasic alterations in the beta 2-adrenoceptor density (Bmax) and cAMP content of these cells. The increase in Bmax after 18 h incubation with IL-2 and PHA was due to the expression of the receptors in a low-affinity state. The stimulatory effect of isoproterenol on adenylate cyclase activity and its effect on cAMP content remained unchanged, indicating uncoupling between the expressed receptors and regulatory Gs-proteins. The addition of phorbolmyristateacetate (PMA), a protein kinase C activator, also caused a biphasic change in beta 2-adrenoceptor density on the surface of the cells. The data point to the involvement of protein kinase C in the mechanism responsible for the increase and subsequent decrease in beta 2-adrenoceptor density seen after activation of T-lymphocytes.