RESUMO
BAY 41-2272 increases guanosine 3', 5'-cyclic monophosphate (cGMP) levels by stimulating soluble guanylate cyclase (sGC). In this study, we evaluated the effect of BAY 41-2272 on human T lymphocyte functions. Pretreating T cells for 24â¯h with BAY 41-2272 at 3⯵M and 30⯵M, followed by activation with 90â¯nM phorbol myristate acetate (PMA), inhibited interferon-gamma (IFN-γ) production, with 3⯵M and 30⯵M BAY causing 16.5-fold and 12.1-fold inhibition, respectively, compared to PMA alone (pâ¯<â¯0.05, one-way ANOVA followed by Tukey's test). We also observed suppressive effects on the expression of CD69, with 30⯵M BAY causing 3.55-fold lower expression than PMA/ionomycin (pâ¯<â¯0.001 one-way ANOVA followed by Tukey's test), and T-bet, with 30⯵M BAY causing 1.47-fold lower expression than PMA/ionomycin (pâ¯<â¯0.05, one-way ANOVA test followed by Tukey's test). Additionally, T lymphocyte proliferation was reduced 2.13-fold and 4.3-fold, respectively, by 3⯵M BAY and 30⯵M BAY compared to PMA/ionomycin (pâ¯<â¯0.01, pâ¯<â¯0.001, one-way ANOVA followed by Tukey's test). BAY 41-2272 inhibits human T lymphocyte function and may be explored as an immunomodulatory drug in patients with autoimmune/inflammatory diseases and lymphoproliferative syndromes.