TXA modulates myeloid and lymphoid cells, as well as plasma cytokines, in the immune response after cardiac surgery. Patients undergoing cardiac surgery were treated with placebo or TXA, and the cellular immune response was characterized using flow cytometry before drug administration, as well as on POD-1 and POD-3. (A) CD83 expression was significantly increased on nonclassical monocytes in the TXA group at POD-3. (B) CD83 on CD1c⁺ cDCs was downregulated to a significantly lower extent in TXA-treated patients at POD-3. (C) TXA treatment also resulted in a significant relative increase in CCR7-expressing CD1c⁺ cDCs. (D) Moreover, TXA reduced expression of the programmed cell death inducing PD-L1 on nonclassical monocytes at POD-3. (E) CD4⁺ T cells were reduced significantly after cardiac surgery, whereby the decrease was significantly greater in the TXA group at POD-1. (F) CD8⁺ Tmem counts were also reduced at POD-1, but they remained reduced only in the TXA-treated patients at POD-3. Expression of the latent TGF-β releasing LAP (G) and CCR7 (H) relative to baseline was significantly lower in TXA-treated patients at POD-3. (I) In contrast, CCR7 expression on NK cells was significantly increased in the TXA group on POD-1. (J) Plasma levels of the proinflammatory cytokine IL-1β were significantly reduced in the TXA group compared with placebo at POD-1. Data represent fold-change from preoperative (preOP) levels and are expressed as mean ± standard error of the mean. Placebo: n = 19, TXA: n = 22. ^#P < .05, ^##P < .01, ^###P < .001, ^####P < .0001 vs preOP, 1-way ANOVA with Dunnett’s correction test for multiple comparisons; *P < .05, placebo vs TXA, 2-tailed Student t test.