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Glucocorticoids induce the expression of CD8α chains on concanavalin A-activated rat CD4+ T cells: Induction is inhibited by rat recombinant interleukin 4

AuthorsRamírez, Francisco ; McKnight, Andrew J.; Silva, Augusto ; Mason, Don
Issue Date1992
PublisherRockefeller University Press
CitationJournal of Experimental Medicine 176(6):1551-1559(1992)
AbstractRat T lymphocytes, activated in vitro with concanavalin A (Con A), were shown by flow cytofluorographic analysis to contain a population of cells that simultaneously expressed CD4 and the α chain of CD8. The inclusion of the glucocorticoid hormone dexamethasone in the culture medium greatly increased both the frequency of these double-positive cells and the level of CD8α chain expression. The level of expression of CD4 was not affected, and the cells that expressed CD8 antigen only also remained unchanged in surface phenotype. Detailed studies demonstrated unequivocally that the CD4+CD8α+ cells were not artifacts produced by the random association of single-positive cells in the flow cytofluorograph, but arose from precursors that were single-positive CD4+ cells before activation. Furthermore, Con A activation of purified CD4+ T cells, in the presence of T cell-depleted accessory cells, showed that CD8+ T cells played no role in the induction process. However, the induction of CD8α chain expression on CD4+ T cells and the enhancement of this expression by dexamethasone were almost completely inhibited by rat recombinant interleukin 4 (IL-4). Detection of mRNA for rat CD8α chain by Northern blot closely paralleled the cell surface expression of CD8α antigen, indicating that dexamethasone and IL-4 had opposing effects on mRNA levels. In contrast, IL-4 and dexamethasone both induced CD8α chain expression on a rat CD4+ T cell clone when this was activated by specific antigen, and, although the effect with IL-4 was relatively weak, it did not antagonize the effect of the glucocorticoid. The possible significance of these results is briefly discussed.
Identifiersdoi: 10.1084/jem.176.6.1551
issn: 0022-1007
e-issn: 1540-9538
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