ArticleScientific reports2017
A teleost CD46 is involved in the regulation of complement activation and pathogen infection.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 16 citations in OpenAlex.
- Edwardsiella tarda TraT is an anti-complement factor and a cellular infection promoter.Communications biology · 2022Article
- Complement C3 and Activated Fragment C3a Are Involved in Complement Activation and Anti-Bacterial Immunity.Frontiers in immunology · 2022Article
- Membrane cofactor protein (MCP; CD46): deficiency states and pathogen connections.Current opinion in immunology · 2021Review
- Integrins meet complement: The evolutionary tip of an iceberg orchestrating metabolism and immunity.British journal of pharmacology · 2021Review
- The Translocation and Assembly Module (TAM) ofFrontiers in microbiology · 2020Article
- Characterization of the Genome Feature and Toxic Capacity of aFrontiers in cellular and infection microbiology · 2019Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In mammals, CD46 is involved in the inactivation of complement by factor I (FI). In teleost, study on the function of CD46 is very limited. In this study, we examined the immunological property of a CD46 molecule (CsCD46) from tongue sole, a teleost species with important economic value. We found that recombinant CsCD46 (rCsCD46) interacted with FI and inhibited complement activation in an FI-dependent manner. rCsCD46 also interacted with bacterial pathogens via a different mechanism to that responsible for the FI interaction, involving different rCsCD46 sites. Cellular study showed that CsCD46 was expressed on peripheral blood leukocytes (PBL) and protected the cells against the killing effect of complement. When the CsCD46 on PBL was blocked by antibody before incubation of the cells with bacterial pathogens, cellular infection was significantly reduced. Consistently, when tongue sole were infected with bacterial pathogens in the presence of rCsCD46, tissue dissemination and survival of the pathogens were significantly inhibited. These results provide the first evidence to indicate that CD46 in teleosts negatively regulates complement activation via FI and protects host cells from complement-induced damage, and that CD46 is required for optimal bacterial infection probably by serving as a receptor for the bacteria.
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