ArticleVirology2006
Evidence that multiple defects in murine DC-SIGN inhibit a functional interaction with pathogens.
Article in Virology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
8 citing papers in PubMed, 20 citations in OpenAlex.
- From structure to function - Ligand recognition by myeloid C-type lectin receptors.Computational and structural biotechnology journal · 2022Review
- Influence of Galectin-3 on the Innate Immune Response during Experimental Cryptococcosis.Journal of fungi (Basel, Switzerland) · 2021Article
- HIV-1 Envelope Glycoproteins Induce the Production of TNF-α and IL-10 in Human Monocytes by Activating Calcium Pathway.Scientific reports · 2018Article
- Ebola virus entry into host cells: identifying therapeutic strategies.Current clinical microbiology reports · 2015Article
- Targeting antigens to dendritic cell receptors for vaccine development.Journal of drug delivery · 2013Review
- A murine DC-SIGN homologue contributes to early host defense against Mycobacterium tuberculosis.The Journal of experimental medicine · 2009Article
- Toll-like receptor 2 and DC-SIGNR1 differentially regulate suppressors of cytokine signaling 1 in dendritic cells during Mycobacterium tuberculosis infection.The Journal of biological chemistry · 2009Article
- HIV-1 gp120 mannoses induce immunosuppressive responses from dendritic cells.PLoS pathogens · 2007Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Certain viruses, bacteria, fungi and parasites target dendritic cells through the interaction with the cellular attachment factor DC-SIGN, making this C-type lectin an attractive target for therapeutic intervention. Studies on DC-SIGN function would be greatly aided by the establishment of a mouse model, however, it is unclear if the murine (m) homologue of human (h) DC-SIGN also binds to pathogens. Here, we investigated the interaction of mDC-SIGN, also termed CIRE, with the Ebolavirus glycoprotein (EBOV-GP), a ligand of hDC-SIGN. We found that mDC-SIGN neither binds EBOV-GP nor enhances infection by reporterviruses pseudotyped with EBOV-GP. Analysis of chimeras between mDC-SIGN and hDC-SIGN provided evidence that determinants in the carbohydrate recognition domain and in the neck domain of mDC-SIGN inhibit a functional interaction with EBOV-GP. Moreover, mDC-SIGN was found be monomeric, suggesting that lack of multimerization, which is believed to be required for efficient pathogen recognition by hDC-SIGN, might be one factor that prevents binding of mDC-SIGN to EBOV-GP. Our results suggest that mDC-SIGN on murine dendritic cells is not an adequate model for pathogen interactions with hDC-SIGN.
Indexed as
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What OpenQuestion holds
Registered trials
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.