Abstract

The present study was undertaken to determine the effect of in vivo hydrocortisone on the kinetics of subpopulations of normal human peripheral blood (PB) thymus-derived (T) cells. Normal volunteers received a single i.v. dose of hydrocortisone, and blood was taken just before, as well as 4, 24, and 48 h after hydrocortisone administration. T cells were purified from each specimen, and proportions and absolute numbers of T lymphocytes bearing receptors for the Fc portion of IgG (T(.G)) and for the Fc portion of IgM (T(.M)) were enumerated by rosetting T cells with bovine erythrocytes which had been coated with either antibovine erythrocyte IgG or IgM. 4 h after i.v. administration of hydrocortisone, T(.M) cells decreased from 52 (+/-5%) to 23 (+/-6%) of PB T cells (P < 0.01) and the absolute number of T(.M) cells decreased from 1,028 (+/-171) per mm(3) to 103 (+/-23) per mm(3) (P < 0.001). In contrast, relative proportion of T(.G) cells increased from 22 (+/-4%) to 66 (+/-7%), while the absolute numbers of T(.G) cells were essentially unchanged (P > 0.2). In vitro studies involving preincubation of T cells with hydrocortisone before rosette determination of T(.G) or T(.M) cells demonstrated that the decrease in absolute numbers of T(.M) cells did not represent hydrocortisone interference with T(.M) rosette formation, nor did it represent a switch of T(.M) cells to T(.G) cells. Thus, administration of hydrocortisone to normal subjects produces a selective depletion from the circulation of T lymphocytes which possess receptors for the Fc portion of IgM (T(.M) cells) and of T cells which possess no detectable F(C) receptor (T(.non-M, non-G) cells). T(.G) cells are relatively resistant to the lymphopenic effect of hydrocortisone. These data clearly demonstrate that in vivo corticosteroids have a differential effect on the kinetics of identifiable and distinct subsets of cells in the human T-cell class.

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