ArticleInfection and immunity2007
Induction of cell signaling events by the cholera toxin B subunit in antigen-presenting cells.
Article in Infection and immunity, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 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
24 citing papers in PubMed, 44 citations in OpenAlex.
- EPICERTIN, an engineered variant of cholera toxin B subunit, promotes survival and a pro-remodeling macrophage phenotype for mucosal healing in colitis.Mucosal immunology · 2026Article
- The Functions of Cholera Toxin Subunit B as a Modulator of Silica Nanoparticle Endocytosis.Toxins · 2023Article
- Bacterial lectin BambL acts as a B cell superantigen.Cellular and molecular life sciences : CMLS · 2021Article
- Review
- Evaluation of the Efficacy of a Cholera-Toxin-BasedVaccines · 2020Article
- The role of lipid species in membranes and cancer-related changes.Cancer metastasis reviews · 2020Review
- The role of PS 18:0/18:1 in membrane function.Nature communications · 2019Review
- Clathrin-independent endocytosis: an increasing degree of complexity.Histochemistry and cell biology · 2018Review
- Article
- CBirTox is a selective antigen-specific agonist of the Treg-IgA-microbiota homeostatic pathway.PloS one · 2017Article
- Pathophysiological mechanisms of diarrhea caused by the Vibrio cholerae O1 El Tor variant: an in vivo study in mice.Virulence · 2016Article
- Gut T cell receptor-γδ(+) intraepithelial lymphocytes are activated selectively by cholera toxin to break oral tolerance in mice.Clinical and experimental immunology · 2015Article
- Immunogenicity of a West Nile virus DIII-cholera toxin A2/B chimera after intranasal delivery.Toxins · 2014Article
- The mucosal adjuvant cholera toxin B instructs non-mucosal dendritic cells to promote IgA production via retinoic acid and TGF-β.PloS one · 2013Article
- The A subunit of Escherichia coli heat-labile enterotoxin functions as a mucosal adjuvant and promotes IgG2a, IgA, and Th17 responses to vaccine antigens.Infection and immunity · 2012Article
- Hemocyte-hemocyte adhesion and nodulation reactions of the greater wax moth, Galleria mellonella are influenced by cholera toxin and its B-subunit.Results in immunology · 2012Article
- Mucosal immunization with a Staphylococcus aureus IsdA-cholera toxin A2/B chimera induces antigen-specific Th2-type responses in mice.Clinical and vaccine immunology : CVI · 2011Article
- Glycosphingolipid functions.Cold Spring Harbor perspectives in biology · 2011Review
- Cholera toxin impairs the differentiation of monocytes into dendritic cells, inducing professional antigen-presenting myeloid cells.Infection and immunity · 2011Article
- Purification and characterization of Yersinia enterocolitica and Yersinia pestis LcrV-cholera toxin A(2)/B chimeras.Protein expression and purification · 2010Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cholera toxin (CT) is one of the most effective and widely studied mucosal adjuvants. Although the ADP-ribosylating A subunit has been implicated in augmenting immune responses, the receptor-binding B subunit (CT-B) has greater immunogenicity and may be a repository of adjuvant activity without potential toxicity. In order to elucidate mechanisms of immune modulation by CT-B alone, primary B cells and macrophages were assessed for responses to CT-B in vitro, as measured by the expression of cell surface markers, cellular signaling events, and cytokine secretion. Increased phosphorylation of multiple signaling molecules, including Erk1/2 and p38, was detected. CT-B also induced transactivation of the transcription elements cyclic AMP-responsive element and NF-kappaB, the latter of which was inhibited by phosphotyrosine inhibition. While specific inhibition of MEK1/2 did not reduce CT-B induction of cell surface marker expression, it did attenuate CT-B-mediated interleukin-6 secretion. These data show that CT-B induces a set of signaling events related to cellular activation, surface molecule expression, and cytokine production that has potential implications for elucidating CT-B adjuvant activity in the absence of enzymatically active holotoxin.
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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.