Abstract
Concanavalin [Con] A-induced [human] suppressor T cells responded to T cell growth factor (TCGF) by proliferation. TCGF abrogated the suppressor activity exerted by these cells on phytohemagglutinin (PHA)- and alloantigen-induced lymphocyte proliferation and on pokeweed mitogen (PWM)-driven Ig secretion. The Con A-activated suppressor T cells absorbed the TCGF activity, preincubation of these active suppressor cells with TCGF abolished their suppressor activity and addition of increasing numbers of Con A-activated T cells reverted the abrogatory effect of TCGF. Con A-induced suppressor T cells probably exert their function by decreasing the available levels of TCGF. Cyclosporin-A (CYA), which inhibits the expression of receptors for TCGF on T cells, also inhibited the suppressor activity as determined in both indicator systems, i.e., PHA- or alloantigen-induced DNA synthesis and PWM-induced Ig synthesis. CYA made Con A-treated T cells unresponsive to TCGF and unable to absorb the growth factor, supporting the notion that CYA inhibits the expression of TCGF receptors on T cells, a mechanism by which this drug seems to abrogate Con A-induced suppressor T cell function.