Fasciola hepatica Immune Regulates CD11c+ Cells by Interacting with the Macrophage Gal/GalNAc Lectin

Ernesto Rodríguez, Paula Carasi, Sofía Frigerio, Valeria da Costa, Sandra van Vliet, Verónica Noya, Natalie Brossard, Yvette van Kooyk, Juan J García-Vallejo, Teresa Freire

Research output: Contribution to journalArticleAcademicpeer-review

Abstract

Fasciolosis, caused byFasciola hepaticaandFasciola gigantica, is a trematode zoonosis of interest in public health and livestock production. Like other helminths,F. hepaticamodulates the host immune response by inducing potent polarized Th2 and regulatory T cell immune responses and by downregulating the production of Th1 cytokines. In this work, we show thatF. hepaticaglycans increase Th2 immune responses by immunomodulating TLR-induced maturation and function of dendritic cells (DCs). This process was mediated by the macrophage Gal/GalNAc lectin (MGL) expressed on DCs, which recognizes the Tn antigen (GalNAc-Ser/Thr) on parasite components. More interestingly, we identified MGL-expressing CD11c+cells in infected animals and showed that these cells are recruited both to the peritoneum and the liver uponF. hepaticainfection. These cells express the regulatory cytokines IL-10, TNFα and TGFβ and a variety of regulatory markers. Furthermore, MGL+CD11c+cells expand parasite-specific Th2/regulatory cells and suppress Th1 polarization. The results presented here suggest a potential role of MGL in the immunomodulation of DCs induced byF. hepaticaand contribute to a better understanding of the molecular and immunoregulatory mechanisms induced by this parasite.

Original languageEnglish
Pages (from-to)264
JournalFrontiers in Immunology: Molecular Innate Immunity
Volume8
DOIs
Publication statusPublished - 2017

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