Helicobacter pylori pediatric infection changes Fc epsilon RI expression in dendritic cells and Treg profile in vivo and in vitro

León M.A.; Palma C.; Hernández C.; Sandoval M.; Cofre C.; Perez-Mateluna G.; Borzutzky A.; Harris P.R.; Serrano C.A.

Abstract

H. pylori infection shows an inverse relationship with allergies. Dendritic cells regulate mucosal immune responses including the induction of T regulatory cells which are fundamental in Helicobacter pylori-induced dampening of allergies. In this respect expression of high-affinity IgE receptor (Fc epsilon RI) has been associated with a regulatory dendritic cell profile. Therefore we aimed to evaluate possible mechanisms by which H. pylori infection might modify atopy in pediatric patients. Here we show that H. pylori-infected children exhibited both increased expression of Fc epsilon RI on peripheral myeloid and plasmacytoid dendritic cells and higher levels of Foxp3 and Latency Associated Peptide on T regulatory cells. Moreover, exposure to H. pylori drove increased Fc epsilon RI expression and IL 10 secretion by both pediatric H. pylori-exposed monocyte derived dendritic cells and T cells. Finally, we show a positive correlation between expression of Fc epsilon RI in circulating myeloid DCs and total Treg cells, suggesting that in children, H. pylori infection may have a modulating role in atopy, mediated by both altered surface expression of Fc epsilon RI on children's DC and an increased T regulatory cell profile. (C) 2019 Institut Pasteur. Published by Elsevier Masson SAS. All rights reserved.

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Título según WOS: Helicobacter pylori pediatric infection changes Fc epsilon RI expression in dendritic cells and Treg profile in vivo and in vitro
Título según SCOPUS: Helicobacter pylori pediatric infection changes Fc?RI expression in dendritic cells and Treg profile in vivo and in vitro
Título de la Revista: MICROBES AND INFECTION
Volumen: 21
Número: 10
Editorial: Elsevier
Fecha de publicación: 2019
Página de inicio: 449
Página final: 455
Idioma: English
DOI:

10.1016/j.micinf.2019.05.001

Notas: ISI, SCOPUS