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The Siglec-E-deficient dendritic cells were defective for TRIF-mediated IFN-beta production in response to E. coli infection.
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This study demonstrated that virulent parasite Leishmania donovani (AG83+Sias) establish a unique sialic acids-mediated binding and subsequent phagocytosis in the host cell through the selective exploitation of siglec-1.
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new data relating to the structure and function of Siglec-E, the major CD33-related Siglec expressed on mouse neutrophils, monocytes, macrophages, and dendritic cells.
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indicate that Siglec-9 affects several different signaling pathways in IL-4-stimulated macrophages, which resulted in enhanced induction of Arg1 in Siglec-9-expressing RAW264 cells
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Competitive ELISA assays confirmed the involvement of sulfated epitopes in the affinity between Siglec-E and cruzipain, probably modified by natural protein environment
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Data indicate a role for neuraminidase 1 (Neu1) in regulating Siglec E protein-toll-like receptor 4 (TLR4) interaction and endotoxemia.
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Siglec-E-deficient macrophages showed a propensity toward a tumor-promoting M2 polarization, indicating a secondary role of CD33-related Siglecs in limiting cancer-promoting inflammation and tumor growth.
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Group B Streptococcus engages an inhibitory Siglec through sialic acid mimicry to blunt innate immune and inflammatory responses in vivo.
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siglec-E functions as an inhibitory receptor of neutrophils via positive regulation of NADPH oxidase activation and ROS production
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These results suggest that sSiglec-9 has an antitumor benefit against MUC1-expressing tumor in the transgenic mice.
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Siglec-9 expressed on immune cells may play a role as a potential counterreceptor for MUC1 and that this signaling may be another MUC1-mediated pathway and function in parallel with a growth factor-dependent pathway.
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Siglec-E is an important negative regulator of neutrophil recruitment to the lung and beta2 integrin-dependent signaling.
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Early murine T-lymphocyte activation is accompanied by a switch from N-Glycolyl- to N-acetyl-neuraminic acid and generation of ligands for siglec-E
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Siglec-E is induced in a MyD88-dependent manner. Once up-regulated, it can control TLR-dependent NF-kappaB antiviral responses by directly inhibiting TLR-induced antiviral cytokine production.
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Siglec-E interacted with the pathogenic Tulahuen strain, but showed a diminished binding to the Tehuantepec strain of Trypanosoma cruzi
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are a family of sialic acid receptor proteins expressed in immune cells, recognize their ligands and play a role in the signal transduction.