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Glucocorticoid receptors and glutamine synthetase in leukemic Sézary cells.

Using a competitive binding assay, we have detected cytoplasmic glucocorticoid receptors in the leukemic cells of several patients with Sezary syndrome, while cells from other patients appear to contain very low or nondetectable receptor levels. The receptors are saturated at approximately 4 × 10-8 m [3H]dexamethasone, and Scatchard analyses of the binding data indicate a high affinity (Kd = 6.9 × 10-9 m). The cytoplasmic receptors are inactivated at 37°, but at 4° they are relatively stable, even in the absence of glucocorticoids. Competition studies have established the specificity of these receptors. Active glucocorticoids such as dexamethasone, prednisolone, and cortisol (50-fold molar excess) completely block [3H]dexamethasone binding, while nonglucocorticoids such as 17β-estradiol and 5α-dihydrotestosterone have no effect at equivalent concentrations. The antiinducer progesterone is also an effective competitor of [3H]dexamethasone binding. The [3H]dexamethasone-receptor complex migrates in linear 5 to 20% sucrose gradients (0.4 m KCI) with a sedimentation coefficient of 4S20,ω. In those cells which contained receptors, the specific activity of glutamine synthetase was increased 2-fold after an 18-hr exposure to dexamethasone (10-6 m), whereas no such increase occurred in cells lacking receptor. The presumptive induction of glutamine synthetase activity may thus serve as a marker for functional receptors in leukemic Sezary cells. Retrospective studies (4 patients) suggest a possible correlation between receptor levels and clinical responsiveness to glucocorticoid therapy.