• 1 January 1981
    • journal article
    • review article
    • Vol. 57  (3) , 379-394
Abstract
The discovery of T cell growth factor (TCGF) has made it possible to routinely grow in tissue culture normal and neoplastic human T cells for long periods and in large amounts. TCGF was recently purified. It is a small protein released by a subset of mature T cells following lectin-antigen activation, which in turn acts upon other T cell subsets that have developed specific receptors for TCGF after lectin-antigen stimulation. Release of TCGF and development of receptors for it appear to be obligatory for the clonal expansion of all activated T cells. Unlike normal T cells, neoplastic T cells respond directly to TCGF requiring no prior in vitro lectin-antigen activation. This led to the development of several new cell lines from patients with T cell leukemias and lymphomas. In some cases, these cells become independent of exogenous TCGF by producing their own growth factor, implying a role for TCGF in the continuous proliferation of these cells. These developments necessitate a reevaluation of some concepts of immunoregulation of T cell activities in terms of production and response to TCGF. This information has clinical implications. A major defect of the athymic nude mouse is the inability to produce TCGF. Some immunosuppressive agents, such as glucocorticosteroids and cyclosporin A, exert their effects on T cells by disrupting the TCGF-T-cell interaction. Some human immune deficiencies might be due to a failure to respond to or to produce TCGF, which in some cases might be corrected by exogenous TCGF.