Abstract

Abstract Helminth infectionsinduce Th2-biased immune responses. Mechanisms involved in this phenomenon are notyet clearly defined, but antigen-presenting cells (APC) playan important role in this process. Dendritic Cells (DC) recognize motifs that are conserved between pathogens mainly through Toll-like receptors(TLR) family, which is the main pathway known to be involved in maturating and inducing inflammatory cytokines in DCs. Most of intracellular pathogens drive Th1 type responses largely through these TLRs. By contrast, the result of the interaction between DCs and helminth parasites is less clear. To dissect mechanisms that lead to immune modulation in experimental cysticercosis, we have used DC exposed to Taenia excreted/secreted glycoproteins and examined their role as APCs, as well as in the modulation of DC responses to pro-inflammatory stimuli. We found that Taenia antigens had the ability to downmodulate DC production of TNF-α and IL-12 in response to several inflammatory molecules such as LPS, CpG and Toxoplasma Ags. Taenia-exposed DC displayed increased ability to suppress IFN-γ production but maintained IL-4 production on CD4+ DO11.10 cells in response to OVA in a STAT6-independent manner. Our results reflect the potential ability of T. crassiceps antigens to modulate DC-inflammatory responses to non-related pro-inflammatory molecules. Work supported by PAPIIT IN208706

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