Dipyridamol inhibits activation of human T lymphocytes in vitro.
The effect of dipyridamol on T-lymphocyte activation was investigated. The drug did not have an irreversible toxic effect on T lymphocytes. Dipyridamol inhibited both PHA- and mumps-stimulated proliferation and the proliferative response in mixed lymphocyte cultures. The drug inhibited PHA-stimulated proliferation independent of the time when it was added during the culture period. The PHA-stimulated expression of interleukin-2 (IL-2) receptors and IL-2 production (at least for low concentrations) was not inhibited. Dipyridamol inhibited IL-2-dependent growth of T cell lines. The drug caused no inhibition when present only during antigenic pulsing.
D002455:Cell Division / Q000187:drug effects; D002478:Cells, Cultured; D004176:Dipyridamole / Q000494:pharmacology*; D006801:Humans; D007376:Interleukin-2 / Q000037:antagonists & inhibitors; D008213:Lymphocyte Activation / Q000187:drug effects*; D010835:Phytohemagglutinins / Q000494:pharmacology; D011971:Receptors, Immunologic / Q000096:biosynthesis; D015375:Receptors, Interleukin-2; D013601:T-Lymphocytes / Q000187:drug effects* / Q000276:immunology
D007376:Interleukin-2; D010835:Phytohemagglutinins; D011971:Receptors, Immunologic; D015375:Receptors, Interleukin-2; D004176:Dipyridamole