ArticlePLoS neglected tropical diseases2015
Trichinella spiralis Paramyosin Binds Human Complement C1q and Inhibits Classical Complement Activation.
Article in PLoS neglected tropical diseases, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 44 citations in OpenAlex.
- Trichinella spiralis serine protease mediates larval invasion of gut epithelium via binding to CK8 and activating RhoA/ROCK1 pathway.PLoS neglected tropical diseases · 2025Article
- Assessing diagnostic, vaccine and therapeutic potential of selectedFood and waterborne parasitology · 2025Review
- Article
- Galactomannan inhibits Trichinella spiralis invasion of intestinal epithelium cells and enhances antibody-dependent cellular cytotoxicity related killing of larvae by driving macrophage polarization.Parasite (Paris, France) · 2024Article
- A novel Trichinella spiralis serine proteinase disrupted gut epithelial barrier and mediated larval invasion through binding to RACK1 and activating MAPK/ERK1/2 pathway.PLoS neglected tropical diseases · 2024Article
- A novel trypsin of Trichinella spiralis mediates larval invasion of gut epithelium via binding to PAR2 and activating ERK1/2 pathway.PLoS neglected tropical diseases · 2024Article
- Trichinella spiralis galectin binding to toll-like receptor 4 induces intestinal inflammation and mediates larval invasion of gut mucosa.Veterinary research · 2023Article
- Binding of Trichinella spiralis C-type lectin with syndecan-1 on intestinal epithelial cells mediates larval invasion of intestinal epithelium.Veterinary research · 2023Article
- Differential Protein Expression ofPathogens (Basel, Switzerland) · 2023Article
- Article
- Microbial evasion of the complement system: a continuous and evolving story.Frontiers in immunology · 2023Review
- Article
- Immunomodulatory and biological properties of helminth-derived small molecules: Potential applications in diagnostics and therapeutics.Frontiers in parasitology · 2022Review
- Article
- The Interactions of Parasite Calreticulin With Initial Complement Components: Consequences in Immunity and Virulence.Frontiers in immunology · 2020Review
- A Multiple Antigen Peptide Vaccine Containing CD4Journal of immunology research · 2020Article
- Article
- Complement Evasion: An Effective Strategy That Parasites Utilize to Survive in the Host.Frontiers in microbiology · 2019Review
- Mapping of the complement C1q binding site on Trichinella spiralis paramyosin.Parasites & vectors · 2018Article
- Trichinella britovi muscle larvae and adult worms: stage-specific and common antigens detected by two-dimensional gel electrophoresis-based immunoblotting.Parasites & vectors · 2018Article
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundTrichinella spiralis expresses paramyosin (Ts-Pmy) as a defense mechanism. Ts-Pmy is a functional protein with binding activity to human complement C8 and C9 and thus plays a role in evading the attack of the host's immune system. In the present study, the binding activity of Ts-Pmy to human complement C1q and its ability to inhibit classical complement activation were investigated. METHODS AND
findingsThe binding of recombinant and natural Ts-Pmy to human C1q were determined by ELISA, Far Western blotting and immunoprecipitation, respectively. Binding of recombinant Ts-Pmy (rTs-Pmy) to C1q inhibited C1q binding to IgM and consequently inhibited C3 deposition. The lysis of antibody-sensitized erythrocytes (EAs) elicited by the classical complement pathway was also inhibited in the presence of rTs-Pmy. In addition to inhibiting classical complement activation, rTs-Pmy also suppressed C1q binding to THP-1-derived macrophages, thereby reducing C1q-induced macrophages migration.
conclusionOur results suggest that T. spiralis paramyosin plays an important role in immune evasion by interfering with complement activation through binding to C1q in addition to C8 and C9.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.