Abstract
GLUCOCORTICOIDS exert widespread suppressive effects on lymphocytes of most species1,2. Sensitivity to the hormones is thought to vary with the state of lymphocyte maturation and differentiation. Immature thymic lymphocytes, for example, are more sensitive than mature thymic-dependent lymphocytes1,3. Furthermore, in vitro studies have suggested that glucocorticoid sensitivity varies with the state of mitogen or antigen-induced activation. Nowell4 observed that prednisolone-21-phosphate reduced the number of mitoses induced in human peripheral blood lymphocytes by phytohaemagglutinin (PHA), and noted that this inhibition required the presence of glucocorticoids during the first 24 h of exposure to PHA. When glucocorticoids were added 48 h after PHA, a time when mitoses had not yet appeared, they had no effect on the number of mitoses measured 2 d later. Tormey et al.5 extended these results to show that prednisolone-21-phosphate inhibited incorporation of radiolabelled thymidine and cytidine into PHA-stimulated lymphocytes, and found that delayed addition of steroid resulted in diminished inhibition.
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SMITH, K., CRABTREE, G., KENNEDY, S. et al. Glucocorticoid receptors and glucocorticoid sensitivity of mitogen stimulated and unstimulated human lymphocytes. Nature 267, 523–526 (1977). https://doi.org/10.1038/267523a0
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DOI: https://doi.org/10.1038/267523a0
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