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A C Tr The presenit study was unldertakein to (letermiinie the effect of in vivo hvdrocortisone on the kinetics of subpopulation s of' iorimial h iimani peripheral 1loo0( (PB) thvmus-derived (T) cells. Normal voluni1teers received a sinigle i.v. (lose of hvdrocortisone, an(l 1)loo0( was takeni juist before, as wvell as 4, 24, anid 48 h after hvcdrocortisone admiinlistrationi. T cells were purified from each specimiieni, anid proportionis and( absolute numbers of T lymphocytes bearing receptors for the Fe portion of' IgG (T.G) an1d fOr the Fe portion of IMNI (T.M) were enumllerated by rosettinig T cells with bovine erv-throcvtes which hacd been coate(d with either antibovine ervthrocyte IgG or IgNI. 4 h after i.v. adiministrationi of hvdrocortisone, T.m cells decrease(d from 52 (5%) to 23 (46%) of PB T cells (P 0.2). In vitro stuidies involving preincubation of T cells with hvdrocortisone before rosette (leteriminiationi of T., or T.M cells demoni- strated that the dlecrease in absolute numnbers of T.M cells did not represenit hvdrocortisone interferenee with T.M rosette formiiation, nor didl it represenit a sw;.,itch of T.M cells to T., cells. Thus, admiiniistration of hydro- cortisone to normnal subjects produces a selective depletion from the circulationi of T lymphocytes which possess receptors for the Fc portion of IgNI (T.M cells) and of T cells which possess no detectal)le Fe receptor (T.noln-M, non--G cells). T.G cells are relatively re- sistaint to the lvmphopenic effect of hvdrocortisonle.
Haynes et al. (Wed,) studied this question.