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  • Title: Posttranscriptional mechanisms of glucocorticoid antiproliferative effects: glucocorticoids inhibit IL-6-induced proliferation of B9 hybridoma cells.
    Author: Almawi WY, Tamim H.
    Journal: Cell Transplant; 2001; 10(2):161-4. PubMed ID: 11332630.
    Abstract:
    Addition of rIL-6 to IL-6-dependent B9 cells starved for IL-6 for 16-20 h stimulated a vigorous proliferative response. Glucocorticoids (GCs), in a concentration-dependent manner, inhibited rIL-6-stimulated proliferation of B9 cells This inhibition was specific for the GCs, evident by the capacity of the GCs, dexamethasone, prednisolone, and hydrocortisone, but not non-GC steroids, to suppress rIL-6-dependent B9 cell proliferation. Furthermore, GC inhibition of IL-6-stimulated B9 cell proliferation was receptor mediated and was abrogated by the GC receptor antagonist, RU486. In addition to their reported effects on inhibition IL-6 expression, the results presented support the notion that GCs also acted distally by suppressing signal transduction through the IL-6 receptor.
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