Thalidomide increases the synthesis of IL-2 in cultures of human mononuclear cells stimulated with Concanavalin-A, Staphylococcal enterotoxin A, and purified protein derivative.

Thalidomide significantly increases the quantity of extracellular IL-2 in cultures of human mononuclear cells stimulated with mitogens or antigen. Cells from 7 donors exposed for 2 h to 4.0 micrograms/ml of thalidomide and stimulated for 16-18 h with 20 micrograms/ml of Concanavalin-A (Con-A) averaged producing 187 +/- 49% more IL-2 than cells stimulated with Con-A alone. In similar experimental procedures and comparisons the pg/ml of IL-2 secreted by thalidomide-treated cells from five donors stimulated with 50 ng/ml of Staphylococcal enterotoxin A (SEA) increased by 159 +/- 32%, and the pg/ml of IL-2 secreted by thalidomide-treated cells from 2 donors stimulated with 5.0 micrograms/ml of purified protein derivative of Mycobacterium tuberculosis increased by 120 +/- 4%. Thalidomide also significantly increases the quantity of intracellular IL-2 in cells stimulated with mitogens. Cells exposed to thalidomide and stimulated with Con-A had an increase in intracellular IL-2 of 130% after 8 h and 157% after 12 h in culture; cells stimulated with SEA had an increase in intracellular IL-2 of 120% after 8 h and 182% after 12 h in culture. Thalidomide did not alter the percent of lymphocytes expressing the alpha-chain of IL-2 receptor, nor did it significantly increase incorporation of [3H]thymidine by cells.