Amilcar FloresCristina Alonso‐VegaEmmanuel HermannMary‐Cruz TorricoNair Alaide Montaño VillarroelFaustino TorricoYves CarlierCarine Truyens2026-03-222026-03-22202310.3390/pathogens12091103https://doi.org/10.3390/pathogens12091103https://andeanlibrary.org/handle/123456789/73932Activated monocytes/macrophages that produce inflammatory cytokines and nitric oxide are crucial for controlling <i>Trypanosoma cruzi</i> infection. We previously showed that uninfected newborns from <i>T. cruzi</i> infected mothers (M+B- newborns) were sensitized to produce higher levels of inflammatory cytokines than newborns from uninfected mothers (M-B- newborns), suggesting that their monocytes were more activated. Thus, we wondered whether these cells might help limit congenital infection. We investigated this possibility by studying the activation status of M+B- cord blood monocytes and their ability to control <i>T. cruzi</i> in vitro infection. We showed that M+B- monocytes have an upregulated capacity to produce the inflammatory cytokine TNF-α and a better ability to control <i>T. cruzi</i> infection than M-B- monocytes. Our study also showed that <i>T. cruzi</i>-specific Abs transferred from the mother play a dual role by favoring trypomastigote entry into M+B- monocytes and inhibiting intracellular amastigote multiplication. These results support the possibility that some M+B- fetuses may eliminate the parasite transmitted in utero from their mothers, thus being uninfected at birth.enTrypanosoma cruziImmunologyBiologyTumor necrosis factor alphaCytokineChagas diseaseAntibodyAmastigoteMonocyteDownregulation and upregulationarticle