Both IDDM and NIDDM are characterized by deviations in peripheral T and B lymphocyte count, T helper : T suppressor ratio, as well as by impaired T suppressor function. These abnormalities may promote insulin antibody and other antibody production, contributing to overt diabetes mellitus development in early stage of the disease. In the present study we explored the eects of cerebrocrast (1,4-dihydropyridine derivative) administration on Con A-and IL-2stimulated tissue lymphocyte blast transformation activity and on the thymus and lymph node mass in normal and streptozotocin (STZ)-induced diabetic rats. It was established that cerebrocrast, administered four times at the doses of 0 . 05 and 0 . 5 mg kg À1 , has long-term (up to 14 days) eects on the immune system and protects against the toxic eect of STZ in STZ-induced diabetic rats, preventing thymus and lymph node mass loss. We conclude that cerebrocrast administration leads to the increase in number and activity of T helper and T suppressor lymphocytes. Glycolysis and DNA synthesis in these cells is augmented under the in¯uence of cerebrocrast administration. We propose that the increase in lymphocyte suppressive activity caused by cerebrocrast administration may prevent the development of IDDM and NIDDM in patients with pre-diabetes, but in patients with early and overt diabetes mellitus the drug administration may prevent the overexpression of insulin antibodies and other antibodies. The eect of cerebrocrast on the de novo production of insulin and IL-2 receptors may be bene®cial for IDDM and NIDDM patients.