Summary:Proliferation of normal human T cells in vitro requires activation of resting T cells by lectin or antigen. This stimulation initiates a series of events which includes elaboration of T cell growth factor (TCGF), expression of TCGF receptors, and, ultimately, cellular proliferation. We sought to determine if TCGF was required for expression of the TCGF receptor in phytohemagglutinin (PHA)‐stimulated normal human T cells. Utilizing dexamethasone (DEX), a known inhibitor of TCGF production, reductions in T cell proliferation, TCGF production, and TCGF receptor expression, as measured by TCGF adsorption and Tac acquisition, were demonstrated after PHA stimulation. When exogenous partially purified TCGF was added to DEX‐containing cultures, the DEX inhibition of proliferation and TCGF receptor expression was completely reversed. These experiments were reproduced utilizing both highly purified TCGF from the Jurkat cell line and purified TCGF synthesized by bacteria from cloned TCGF DNA. Short‐term experiments showed TCGF to be capable of restoring Tac antigen expression after DEX inhibition in the absence of cellular proliferation. These results indicate that TCGF is required for optimal expression of Tac antigen—associated TCGF receptors in PHA‐activated T cells.