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Maternal immunological imprinting/priming of infant immune responses

Besides the direct effects of transferred antibodies, the elements mentioned above (see section: Main biorelevant transferred molecules) can imprint/prime the fetal/neonatal immune system with long-term unexpected consequences (epigenetic effects). They can promote specific immunological memory or, conversely, immune tolerance, increasing resistance or susceptibility to further T. cruzi (re)infection, respectively (see section: Fetal/neonatal factors involved in the development of congenital Chagas disease), leading to more or less severe clinical forms of Chagas disease. Moreover, this imprinting in early life can also have consequences for responses toward other infections or vaccinations (reviewed in Refs. [116,117]). Our team showed that uninfected infants from infected mothers displayed stronger type 1 response to BCG (producing IFN-y) and that congenitally infected infants developed this stronger response to hepatitis B, diphtheria, and tetanus vaccines, as well as enhanced antibody production to hepatitis B vaccine, compared to controls from uninfected mothers.118 This might be related to an activation of fetal/neonatal dendritic cells (DCs) (induced by soluble parasite-derived molecules transferred from their mother).119,120

Fetal/neonatal factors involved in the development of congenital Chagas disease

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