Morphine depression of T cell E-rosetting: definition of the process

Abstract

Two kinetic assays were developed to assess opiate effects on rates of T cell E-rosetting. The first adopted the thermal conditions of active E-rosetting assays (varying between 37 and 23 C) whereas the second incorporated cooler thermal conditions (varying between 0 and 29 C). In vitro treatment of lymphocytes with morphine depressed E-receptor levels and E-rosetting in both assays. With the 0-29 C procedure early stages of E-rosette formation were characterized by phase transition kinetics indicative of sequential gain and loss of E-rosettes. Assay thermal and erythrocyte (E) to T cell contact conditions, and the inclusion of morphine during E-rosetting, were independent variables that coordinately modulated the expression of phase transitions. Phase transitions were also noted during capping of total T cell E-rosettes at 37 C. The reason for phase transitions appears to be that T cells undergo sequential cycling of E-receptors, increasing because of the new expression of dormant E-receptors as the result of E-receptor microdisplacement and decreasing because E-rosettes are lost owing to patching and capping processes. According to this construction of the E-rosetting process, morphine inhibits E-rosetting and modulates expression of phase transitions by interfering with E-receptor microdisplacement processes. Presumably this interference by morphine is mediated through alteration of membrane fluidity and promotion of E-receptor coupling (and/or inhibition of uncoupling) to a transducer-effector component within the cell membrane. These findings and conclusions are specifically relevant to immunoregulatory processes and are also helpful for understanding the general nature of biological and physiological responses associated with receptor-ligand interactions.