ArticleBMC immunology2018
The excretory-secretory products of Echinococcus granulosus protoscoleces stimulated IL-10 production in B cells via TLR-2 signaling.
Article in BMC immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed.
- First analysis of Spirometra mansoni excretory-secretory proteins by the 4D-DIA method.Parasite (Paris, France) · 2026Article
- Article
- Regulatory B cells in parasitic infections: roles and therapeutic potential.Parasitology research · 2025Review
- Characterisation of extracellular vesicles isolated from hydatid cyst fluid and evaluation of immunomodulatory effects on human monocytes.Journal of cellular and molecular medicine · 2023Article
- Evaluation of the Local Immune Response to Hydatid Cysts in Sheep Liver.Veterinary sciences · 2023Article
- Immune and Genomic Analysis of Boxer Dog Breed and Its Relationship withVeterinary sciences · 2022Article
- Article
- Echinococcus multilocularis specific antibody, systemic cytokine, and chemokine levels, as well as antigen-specific cellular responses in patients with progressive, stable, and cured alveolar echinococcosis: A 10-year follow-up.PLoS neglected tropical diseases · 2022Article
- Characterization of a novel cysteine protease inhibitor inFrontiers in immunology · 2022Article
- The non-oral infection of larvalFrontiers in immunology · 2022Article
- Transcriptomic Profiles of Splenic CD19Frontiers in veterinary science · 2022Article
- Therapeutic Efficacy of Excretory-Secretory Products ofFrontiers in cellular and infection microbiology · 2021Article
- Use of Toll-Like Receptor (TLR) Ligation to Characterize Human Regulatory B-Cells Subsets.Methods in molecular biology (Clifton, N.J.) · 2021Article
- Immunometabolism: Towards a Better Understanding the Mechanism of Parasitic Infection and Immunity.Frontiers in immunology · 2021Review
- Metabolomics Analysis of Splenic CD19Frontiers in veterinary science · 2021Article
- Parasite-Derived Excretory-Secretory Products Alleviate Gut Microbiota Dysbiosis and Improve Cognitive Impairment Induced by a High-Fat Diet.Frontiers in immunology · 2021Article
- Recent advances on innate immune pathways related to host-parasite cross-talk in cystic and alveolar echinococcosis.Parasites & vectors · 2020Review
- TLR-2-mediated metabolic reprogramming participates in polyene phosphatidylcholine-mediated inhibition of M1 macrophage polarization.Immunologic research · 2020Article
- Microarray Analysis of lncRNA and mRNA Reveals Enhanced Lipolysis Along With Metabolic Remodeling in Mice Infected With LarvalFrontiers in physiology · 2020Article
- Comprehensive Analysis of Non-coding RNA Profiles of Exosome-Like Vesicles From the Protoscoleces and Hydatid Cyst Fluid ofFrontiers in cellular and infection microbiology · 2020Article
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Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundExcretory-secretory products released by Echinococcus granulosus protoscoleces (EgPSC-ESPs) are well-known to regulate T cell responses. However, their direct influence on the differentiation of B cell subsets remains largely elusive. This study investigated the effects of EgPSC-ESPs on the differentiation of IL-10-producing B cells (B10), and explored the possible role of Toll-like receptor 2 (TLR-2) signaling in this process.
resultsIn comparison to phosphate buffered saline (PBS), B cells exposed to the excretory-secretory products (ESPs) generated higher percentages of B10 cells, with higher expression of IL-10 mRNA, and larger amount of IL-10 production, which were in a dose dependent way. The mRNA and protein expression of TLR-2 in the ESPs-stimulated B cells were significantly higher than those in PBS, which was consistent to the results in B cells isolated from EgPSC infected mice. Moreover, TLR-2
conclusionOverall, this study revealed that TLR-2 signaling was required for B10 induction mediated by EgPSC-ESPs, which might be an immunomodulatory target against the parasite infection.
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