TXA induces changes to the cellular immune profile in cardiac surgery patients, consistent with enhanced immune activation, selectively in patients without diabetes. Results obtained with flow cytometry were analyzed separately for diabetic and nondiabetic patients. Consistent with our findings on infection outcome, the activation marker CD83 was enhanced by TXA on several myeloid subsets (classical [A] and intermediate [B] monocytes and CD1c⁺ cDCs [C]) at POD-3 in patients without diabetes, whereas the immunosuppressive marker PD-L1 was downregulated on CD1c⁺ cDCs (D) and nonclassical monocytes (E). (G-L) In contrast, these effects were not seen in the diabetic cohort. In fact, PD-L1 even exhibited increased expression (significant in nonclassical monocytes [K], nonsignificant in CD1c⁺ cDCs [J]) at POD-1. In addition, expression of the immunosuppressive marker LAP on Tregs was significantly reduced by TXA on POD-3 in patients without diabetes (F) but not in patients with diabetes (L). Data represent fold-change from preoperative (preOP) levels and are expressed as mean ± standard error of the mean. Placebo: n = 11, TXA: n = 16 (patients without diabetes); placebo: n = 8, TXA: n = 6 (patients with diabetes). *P < .05, **P < .01, 2-tailed Student t test. ns, not significant.