CCA (disodium 4-chloro-2,2'-iminodibenzoate) inhibits progression of human T cell proliferation triggered by PHA.

The effect of the anti-rheumatic drug CCA (disodium 4-chloro-2,2'-iminodibenzoate) on the proliferation of T cells activated by PHA was examined. Cell cycle analysis showed that CCA blocked the transition of the cells from G1 to S (progression), but had little effect on the G0----G1 transition (initiation). CCA had no significant effect on IL-2 receptor expression, an early G1 event, but did inhibit transferrin receptor expression, a late G1 event. CCA did not inhibit IL-2 production by PHA-activated T cells, but did block IFN-gamma production at 72 hr after the stimulation. CCA failed to inhibit c-myc mRNA induction, but did delay the decrease in c-myc mRNA levels that normally occurs with the onset of DNA synthesis. These results indicate that CCA inhibits the progression, but not initiation, of human T cell proliferation.