PREDNISONE-RESPONSIVE APLASTIC-ANEMIA - MECHANISM OF GLUCOCORTICOID ACTION

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  • 1 January 1979
    • journal article
    • research article
    • Vol. 54  (2) , 322-333
Abstract
Serial agar cultures (CFU-C) were performed using marrow cells from a patient with prednisone-responsive aplastic anemia and from 5 patients with prednisone-resistant aplasia. Colony growth was decreased in all patients. Cortisol (10-7-10-4 M) significantly enhanced colony growth in the prednisone-responsive patient but failed to enhance colony growth in the remaining 5 patients. Further studies in the responsive patient indicated that colony growth was enhanced by depleting T [thymus-derived] lymphocytes from the marrow cells, colony growth of T cell-depleted marrow cells was inhibited by autologous peripheral blood lymphocytes (PBL), cortisol failed to enhance colony growth of T cell-depleted marrow cells, PBL and PBL-conditioned medium inhibited colony growth of autologous and allogeneic marrow cells, but neither cortisol-treated PBL nor T cell-depleted PBL were inhibitory. Serial cultures in the responsive patient showed that colony growth normalized during remission when suppressor cells were absent and that colony growth was subnormal during a later relapse when cortisol-resistant suppressor cells were present. In this prednisone-responsive patient, cortisol-sensitive T lymphocytes suppressed granulopoiesis in vitro. Aplastic anemia in this patient is apparently immunologically mediated and prednisone therapy apparently enhanced hemopoiesis in vivo by inhibiting the suppressor T lymphocytes.