EFFECT OF DEXAMETHASONE ON T-CELL RECEPTOR CD3 EXPRESSION/

Glucocorticoid hormones (GCH) are anti-inflammatory and immunosuppress ive agents that inhibit T-cell growth and activation. Since the T-cell receptor (TCR)/CD3 complex mediates T-lymphocyte activation, we studi ed the effect of in vitro dexamethasone (DEX), a synthetic GCH, on TCR /CD3 expression. DEX-treatment of a hybridoma T-cell line and normal u n-transformed T-cell clones induced a decrease of the TCR/CD3 membrane expression after 4 days. After 4 weeks, TCR/CD3 was undetectable. How ever, the amount of mRNAs coding TCR/CD3 chains, including TCR alpha, TCR beta, CD3 gamma, CD3 delta and CD3 epsilon, as well as the amount of CD3 epsilon protein, a major component of the complex, were unalter ed. By contrast, a decrease of the mRNAs deriving from the TCR zeta ge ne locus, as well as of the TCR zeta protein which is responsible for the membrane expression of the TCR/CD3 complex, was induced. These dat a suggest that the down-modulation of TCR expression is due to the dim inution of TCR zeta gene products in DEX-treated cells.