Abstract
An immunosuppressive cyclic polypeptide, cyclosporin A (CyA), isolated originally from 2 species of fungi, prolongs organ allograft survival in several species [of animals]. Virtually nothing is known about the pharmacokinetics of this substance and its mode of action in man. The impact of CyA on T-dependent and T-independent Ig synthesis of human blood leukocytes in vitro and on the proliferating capcity of the interacting lymphoid cell populations (T cells, B cells T.mu. [.mu.-chain receptor-bearing T] and T.gamma. [.gamma.-chain receptor-bearing T] cells) was quantified. CyA inhibited all responses at approximately equal concentrations. The blast cells rather than resting lymphocytes and/or Ig-synthesizing plasma cells were incapacitated by the drug. As the phagocytosis of accessory macrophages was inhibited only at a 100-1000-fold higher drug concentration, CyA apparently has a relatively specific direct effect on human T and B blast cells in vitro.