ArticlePloS one2014
Bordetella adenylate cyclase toxin differentially modulates toll-like receptor-stimulated activation, migration and T cell stimulatory capacity of dendritic cells.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 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.
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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
20 citing papers in PubMed, 28 citations in OpenAlex.
- Post-exposure booster vaccination recalls vaccine-induced memory and accelerates Bordetella pertussis clearance in murine lungs and trachea.Scientific reports · 2026Article
- Limited response of primary nasal epithelial cells toMicrobiology spectrum · 2025Article
- cAMP signaling ofmSphere · 2024Article
- Delivery ofFrontiers in immunology · 2023Article
- Pertussis toxin suppresses dendritic cell-mediated delivery of B. pertussis into lung-draining lymph nodes.PLoS pathogens · 2022Article
- The Fim and FhaB adhesins play a crucial role in nasal cavity infection and Bordetella pertussis transmission in a novel mouse catarrhal infection model.PLoS pathogens · 2022Article
- Pathogenicity and virulence ofVirulence · 2021Review
- Adenylate Cyclase Toxin Tinkering With Monocyte-Macrophage Differentiation.Frontiers in immunology · 2020Review
- Bioengineering ofToxins · 2018Review
- Non-specific Effects of Live Attenuated Pertussis Vaccine Against Heterologous Infectious and Inflammatory Diseases.Frontiers in immunology · 2018Review
- What Is Wrong with Pertussis Vaccine Immunity? Inducing and Recalling Vaccine-Specific Immunity.Cold Spring Harbor perspectives in biology · 2017Review
- Phosphoproteomics of cAMP signaling of Bordetella adenylate cyclase toxin in mouse dendritic cells.Scientific reports · 2017Article
- Review
- Bordetella Adenylate Cyclase-Hemolysin Toxins.Toxins · 2017Review
- Cyclic AMP-Elevating Capacity of Adenylate Cyclase Toxin-Hemolysin Is Sufficient for Lung Infection but Not for Full Virulence of Bordetella pertussis.Infection and immunity · 2017Article
- Dendritic cell migration in health and disease.Nature reviews. Immunology · 2017Review
- Bordetella pertussis: new concepts in pathogenesis and treatment.Current opinion in infectious diseases · 2016Review
- Plasmacytoid dendritic cell-derived IFNα modulates Th17 differentiation during early Bordetella pertussis infection in mice.Mucosal immunology · 2016Article
- Regulatory T-Cell-Mediated Suppression of Conventional T-Cells and Dendritic Cells by Different cAMP Intracellular Pathways.Frontiers in immunology · 2016Review
- Severe, but not mild heat-shock treatment induces immunogenic cell death in cancer cells.OncoimmunologyArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Adenylate cyclase toxin (CyaA) is a key virulence factor of the whooping cough agent Bordetella pertussis. The toxin targets CD11b-expressing phagocytes and delivers into their cytosol an adenylyl cyclase (AC) enzyme that subverts cellular signaling by increasing cAMP levels. In the present study, we analyzed the modulatory effects of CyaA on adhesive, migratory and antigen presenting properties of Toll-like receptor (TLR)-activated murine and human dendritic cells (DCs). cAMP signaling of CyaA enhanced TLR-induced dissolution of cell adhesive contacts and migration of DCs towards the lymph node-homing chemokines CCL19 and CCL21 in vitro. Moreover, we examined in detail the capacity of toxin-treated DCs to induce CD4(+) and CD8(+) T cell responses. Exposure to CyaA decreased the capacity of LPS-stimulated DCs to present soluble protein antigen to CD4+ T cells independently of modulation of co-stimulatory molecules and cytokine production, and enhanced their capacity to promote CD4(+)CD25(+)Foxp3(+) T regulatory cells in vitro. In addition, CyaA decreased the capacity of LPS-stimulated DCs to induce CD8(+) T cell proliferation and limited the induction of IFN-γ producing CD8(+) T cells while enhancing IL-10 and IL-17-production. These results indicate that through activation of cAMP signaling, the CyaA may be mobilizing DCs impaired in T cell stimulatory capacity and arrival of such DCs into draining lymph nodes may than contribute to delay and subversion of host immune responses during B. pertussis infection.
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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.