This article discusses the role of T cell growth factor (TCGF) in T cell proliferation and its interaction with specific receptors. The study shows that TCGF is essential for T cell proliferation, and its effects are dependent on the concentration of TCGF available. TCGF promotes the proliferation of antigen- or lectin-activated T cells but has no mitogenic effect on unstimulated lymphocytes, activated B cells, or cells of other lineages. The study also demonstrates that TCGF interacts with activated T cells through specific membrane binding sites, and that these binding sites are high-affinity and TCGF-specific. The study describes the development of a radiolabeled TCGF binding assay, which was used to show that only TCGF-responsive T cells express high-affinity, TCGF-specific binding sites. The binding characteristics and the close correlation between the binding and biological response curves support the notion that TCGF exerts its effects on activated T cells through a cellular receptor, similar to polypeptide hormones. The study also examines the binding of TCGF to various cell types, including murine and human cells, and finds that the binding is specific to T cell blasts and TCGF-dependent T cell lines. The binding is rapid and largely reversible, and the dissociation constant is only apparent, as processes of internalization and/or degradation may occur during the time used to measure binding. The study also compares the biological activity of TCGF with its binding to various cell types and finds that the concentration of TCGF that stimulates a given fraction of the maximum CTLL proliferation is remarkably similar to the concentration that results in the same fraction of occupied receptor sites. This finding supports the conclusion that the biological response is nearly proportional to the TCGF-binding site occupancy. The study concludes that the binding site detected in these studies is on the receptor through which the biological effects of TCGF are initiated. The findings suggest that it will be possible to apply a quantitative approach to physiological and pathophysiological studies of an immunologically important lymphokine and its receptor. The study also highlights the importance of TCGF-specific binding sites in T cell clonal expansion and the need for further research to understand the role of TCGF in various disease states.This article discusses the role of T cell growth factor (TCGF) in T cell proliferation and its interaction with specific receptors. The study shows that TCGF is essential for T cell proliferation, and its effects are dependent on the concentration of TCGF available. TCGF promotes the proliferation of antigen- or lectin-activated T cells but has no mitogenic effect on unstimulated lymphocytes, activated B cells, or cells of other lineages. The study also demonstrates that TCGF interacts with activated T cells through specific membrane binding sites, and that these binding sites are high-affinity and TCGF-specific. The study describes the development of a radiolabeled TCGF binding assay, which was used to show that only TCGF-responsive T cells express high-affinity, TCGF-specific binding sites. The binding characteristics and the close correlation between the binding and biological response curves support the notion that TCGF exerts its effects on activated T cells through a cellular receptor, similar to polypeptide hormones. The study also examines the binding of TCGF to various cell types, including murine and human cells, and finds that the binding is specific to T cell blasts and TCGF-dependent T cell lines. The binding is rapid and largely reversible, and the dissociation constant is only apparent, as processes of internalization and/or degradation may occur during the time used to measure binding. The study also compares the biological activity of TCGF with its binding to various cell types and finds that the concentration of TCGF that stimulates a given fraction of the maximum CTLL proliferation is remarkably similar to the concentration that results in the same fraction of occupied receptor sites. This finding supports the conclusion that the biological response is nearly proportional to the TCGF-binding site occupancy. The study concludes that the binding site detected in these studies is on the receptor through which the biological effects of TCGF are initiated. The findings suggest that it will be possible to apply a quantitative approach to physiological and pathophysiological studies of an immunologically important lymphokine and its receptor. The study also highlights the importance of TCGF-specific binding sites in T cell clonal expansion and the need for further research to understand the role of TCGF in various disease states.