Posttranscriptional mechanisms of glucocorticoid antiproliferative effects: Glucocorticoids inhibit IL-6-induced proliferation of B9 hybridoma cells

Addition of rIL-6 to IL-6-dependent B9 cells starved for IL-6 for 16-20 h s timulated a vigorous proliferative response. Glucocorticoids (GCs), in a co ncentration-dependent manner, inhibited rIL-6-stimulated proliferation of B 9 cells This inhibition was specific for the GCs, evident by the capacity o f the GCs, dexamethasone, prednisolone, and hydrocortisone. but not non-GC steroids, to suppress rIL-6-dependent B9 cell proliferation. Furthermore, G C inhibition of IL-6-stimulated B9 cell proliferation was receptor mediated and was abrogated by the GC receptor antagonist, RU486. In addition to the ir reported effects on inhibition IL-6 expression, the results presented su pport the notion that GCs also acted distally by suppressing signal transdu ction through the IL-6 receptor.