Transcortin modulates the effect of cortisol on mitogen-induced lymphocyte proliferation and immunoglobulin production.
In the present study we investigated whether transcortin modulates the in vitro effects of cortisol on the proliferation of human peripheral blood mononuclear cells (PBMC) stimulated by different mitogens and on mitogen-induced polyclonal immunoglobulin production. Physiological doses of cortisol (10-1000 nM) strongly inhibited the proliferation of PBMC stimulated by the monoclonal antibody OKT3 or by phytohemagglutinin. Addition of pure cortisol-free transcortin significantly reduced these inhibitory effects in a dose dependent manner. Transcortin (1 microM) caused a 3- to 4-fold reduction of the effects of 100 nM cortisol. Transcortin alone had no influence on the proliferation of stimulated PBMC. Polyclonal immunoglobulin production by PBMC stimulated with pokeweed mitogen was enhanced by physiological does of cortisol. A concentration of 100 nM cortisol caused an increase of immunoglobulin G and M production of 81 and 55% respectively. This effect was abolished by addition of 1 microM transcortin to the cultures, whereas transcortin alone had no effect. These results indicate that an evaluation of the effect of corticoids on lymphoid tissues should be based on the free cortisol level rather than on the total cortisol concentration.
D000328:Adult; D002478:Cells, Cultured; D006801:Humans; D006854:Hydrocortisone / Q000494:pharmacology*; D007136:Immunoglobulins / Q000096:biosynthesis*; D008213:Lymphocyte Activation / Q000187:drug effects*; D008297:Male; D008875:Middle Aged; D011043:Pokeweed Mitogens / Q000494:pharmacology; D014156:Transcortin / Q000494:pharmacology*
D007136:Immunoglobulins; D011043:Pokeweed Mitogens; D014156:Transcortin; D006854:Hydrocortisone