TY - JOUR A2 - Landa, Abraham AU - Montero-Barrera, Daniel AU - Valderrama-Carvajal, Héctor AU - Terrazas, César A. AU - Rojas-Hernández, Saúl AU - Ledesma-Soto, Yadira AU - Vera-Arias, Laura AU - Carrasco-Yépez, Maricela AU - Gómez-García, Lorena AU - Martínez-Saucedo, Diana AU - Becerra-Díaz, Mireya AU - Terrazas, Luis I. PY - 2015 DA - 2015/01/15 TI - The Macrophage Galactose-Type Lectin-1 (MGL1) Recognizes Taenia crassiceps Antigens, Triggers Intracellular Signaling, and Is Critical for Resistance to This Infection SP - 615865 VL - 2015 AB - C-type lectins are multifunctional sugar-binding molecules expressed on dendritic cells (DCs) and macrophages that internalize antigens for processing and presentation. Macrophage galactose-type lectin 1 (MGL1) recognizes glycoconjugates expressing Lewis X structures which contain galactose residues, and it is selectively expressed on immature DCs and macrophages. Helminth parasites contain large amounts of glycosylated components, which play a role in the immune regulation induced by such infections. Macrophages from MGL1−/− mice showed less binding ability toward parasite antigens than their wild-type (WT) counterparts. Exposure of WT macrophages to T. crassiceps antigens triggered tyrosine phosphorylation signaling activity, which was diminished in MGL1−/− macrophages. Following T. crassiceps infection, MGL1−/− mice failed to produce significant levels of inflammatory cytokines early in the infection compared to WT mice. In contrast, MGL1−/− mice developed a Th2-dominant immune response that was associated with significantly higher parasite loads, whereas WT mice were resistant. Flow cytometry and RT-PCR analyses showed overexpression of the mannose receptors, IL-4Rα, PDL2, arginase-1, Ym1, and RELM-α on MGL1−/− macrophages. These studies indicate that MGL1 is involved in T. crassiceps recognition and subsequent innate immune activation and resistance. SN - 2314-6133 UR - https://doi.org/10.1155/2015/615865 DO - 10.1155/2015/615865 JF - BioMed Research International PB - Hindawi Publishing Corporation KW - ER -