Abstract
CCA [N- (2-carboxyphenyl) -4-chloroanthra-nilic acid] at 50-100 μg/ml markedly suppressed the PFC response when an optimal amount of antigen (SRBC) was present in the culture, while the drug did not suppress but enhanced the immune response in conditions where spleen cells were cultured with suboptimal amount of the antigen. On the other hand, the PFC response to DNP-Ficoll (a thymus-independent antigen) was not influenced by CCA. CCA, itself did not show mitogenic activity, but augmented the proliferative response caused by Con A. The proliferative response to a B-cell mitogen, LPS, however, was not affected by addition of 1-50 μg/ml CCA. Oral admiministration of CCA (10 mg/kg) increased the primary PFC response to TNP-HGG or SRBC in normal mice, but suppressed it in NZB/WF1, The secondary antibody response to SRBC, however, was slightly sup-pressed by repeated administration of CCA between the first and second immunization. Moreover, the artificially enhanced antibody response by the injection of colchicine was tend to be restored to the normal level by CCA administration. Thus, the present experiments and other findings suggested that CCA might be a compound having im-munopharmacological profile as an immuno modulator sensitive to T-cell population. It would be expected that this drug can be applied not only to rheumatoid arthritis but also other immune diseases due to T-cell disfunctions.
