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Clinical and Developmental Immunology
Volume 2013, Article ID 981468, 9 pages
Clinical Study

Cysticerci Drive Dendritic Cells to Promote In Vitro and In Vivo Tregs Differentiation

1Instituto Nacional de Neurología y Neurocirugía, Insurgentes Sur 3877, Col. La Fama, 14269 México, DF, Mexico
2Unidad Periférica para el Estudio de Neuroinflamación del Instituto de Investigaciones Biomédicas de la UNAM en el Instituto Nacional de Neurología Neurocirugía, Insurgentes Sur 3877, Col. La Fama, 14269 México, DF, Mexico
3Instituto de Investigaciones Biomédicas, Universidad Nacional Autónoma de México, 04510 México, DF, Mexico
4Departamento de Genómica Computacional, Instituto Nacional de Medicina Genómica, INMEGEN. Periférico Sur 4809, Arenal Tepepan, 14610 México, DF, Mexico
5Unidad de Genotipificación y Análisis de Expresión Affymetrix, INMEGEN, Periférico Sur 4809, Arenal Tepepan, 14610 México, DF, Mexico

Received 1 March 2013; Accepted 24 April 2013

Academic Editor: Arnon Nagler

Copyright © 2013 Laura Adalid-Peralta et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Regulatory T cells (Tregs) play a crucial role in immune homeostasis. Treg induction is a strategy that parasites have evolved to modulate the host’s inflammatory environment, facilitating their establishment and permanence. In human Taenia solium neurocysticercosis (NC), the concurrence of increased peripheral and central Treg levels and their capacity to inhibit T cell activation and proliferation support their role in controlling neuroinflammation. This study is aimed at identifing possible mechanisms of Treg induction in human NC. Monocyte-derived dendritic cells (DC) from healthy human donors, cocultivated with autologous CD4+ naïve cells either in the presence or absence of cysticerci, promoted CD25highFoxp3+ Treg differentiation. An increased Treg induction was observed when cysticerci were present. Moreover, an augmentation of suppressive-related molecules (SLAMF1, B7-H1, and CD205) was found in parasite-induced DC differentiation. Increased Tregs and a higher in vivo DC expression of the regulatory molecules SLAMF1 and CD205 in NC patients were also found. SLAMF1 gene was downregulated in NC patients with extraparenchymal cysticerci, exhibiting higher inflammation levels than patients with parenchymal parasites. Our findings suggest that cysticerci may modulate DC to favor a suppressive environment, which may help parasite establishment, minimizing the excessive inflammation, which may lead to tissue damage.