Abstract
Publisher Summary Typical changes in the immune system because of acute stress include a lymphocytosis, with marked changes in natural killer and T-suppressor cells and more modest effects on T-helper cells. This chapter presents data from two separate studies that were designed to determine β 2 -adrenergic receptor and catecholamine involvement in lymphocyte subset redistribution following acute sympathetic activation and whether cellular adhesion molecules (CAMs) expression on lymphocytes might influence this phenomenon. Subjects were studied following both a psychologic and an exercise stressor. These studies sought to identify adrenergic and CAMs involvement in lymphocytosis following acute immune activation. The studies found that an individual's initial sympathetic state (baseline catecholamines and β 2 -adrenergic receptors) and the magnitude of sympathetic (catecholamine) activation are important factors underlying lymphocyte subset redistribution. The findings also suggest that experimental stress results in differential expression of CAMs on lymphocytes and that CAM expression may influence β -adrenergic effects. For example, the presence or absence of L-selectin on T-suppressor cells determined their post exercise distribution in circulation, with those expressing L-selectin remaining unchanged and those not expressing L-selectin showing a marked redistribution. In addition, only those T-suppressor cells not expressing L-selectin showed a significant attenuating effect of propranolol. These results suggest that L-selectin expression on T-suppressor cells inhibits the effects of sympathetic activation and β blockade.
Published Version
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