ArticleInfection and immunity2009
Cholera toxin and Escherichia coli heat-labile enterotoxin, but not their nontoxic counterparts, improve the antigen-presenting cell function of human B lymphocytes.
Article in Infection and immunity, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 31 citations in OpenAlex.
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- rBCG-LTAK63 enhances protection against tuberculosis by inducing autophagy and circadian gene regulation.Frontiers in immunology · 2025Article
- Nanoparticles and Antiviral Vaccines.Vaccines · 2023Review
- SARS-CoV-2: Immunity, Challenges with Current Vaccines, and a Novel Perspective on Mucosal Vaccines.Vaccines · 2023Review
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- GPR174 signals via GProceedings of the National Academy of Sciences of the United States of America · 2022Article
- Attacking the Intruder at the Gate: Prospects of Mucosal Anti SARS-CoV-2 Vaccines.Pathogens (Basel, Switzerland) · 2022Review
- Fentanyl conjugate vaccine by injected or mucosal delivery with dmLT or LTA1 adjuvants implicates IgA in protection from drug challenge.NPJ vaccines · 2021Article
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- Requirement for Cyclic AMP/Protein Kinase A-Dependent Canonical NFκB Signaling in the Adjuvant Action of Cholera Toxin and Its Non-toxic Derivative mmCT.Frontiers in immunology · 2019Article
- The Mucosal Vaccine Adjuvant LT(R192G/L211A) or dmLT.mSphere · 2018Review
- The B subunit of Escherichia coli heat-labile toxin alters the development and antigen-presenting capacity of dendritic cells.Journal of cellular and molecular medicine · 2015Article
- Escherichia coli heat-labile detoxified enterotoxin modulates dendritic cell function and attenuates allergic airway inflammation.PloS one · 2014Article
- Cholera toxin induces a shift from inactive to active cyclooxygenase 2 in alveolar macrophages activated by Mycobacterium bovis BCG.Infection and immunity · 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
- Article
- Cholera toxin impairs the differentiation of monocytes into dendritic cells, inducing professional antigen-presenting myeloid cells.Infection and immunity · 2011Article
- Cholera-like enterotoxins and Regulatory T cells.Toxins · 2010Review
- Review
- Review
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
B lymphocytes play an important role in the immune response induced by mucosal adjuvants. In this study we investigated the in vitro antigen-presenting cell (APC) properties of human B cells upon treatment with cholera toxin (CT) and Escherichia coli heat-labile enterotoxin (LT) and nontoxic counterparts of these toxins, such as the B subunit of CT (CT-B) and the mutant of LT lacking ADP ribosyltransferase activity (LTK63). Furthermore, forskolin (FSK), a direct activator of adenylate cyclase, and cyclic AMP (cAMP) analogues were used to investigate the role of the increase in intracellular cAMP caused by the A subunit of CT and LT. B lymphocytes were cultured with adjuvants and polyclonal stimuli necessary for activation of B cells in the absence of CD4 T cells. Data indicated that treatment with CT, LT, FSK, or cAMP analogues, but not treatment with CT-B or LTK63, upregulated surface activation markers on B cells, such as CD86 and HLA-DR, and induced inhibition of the proliferation of B cells at early time points, while it increased cell death in long-term cultures. Importantly, B cells treated with CT, LT, or FSK were able to induce pronounced proliferation of both CD4(+) and CD8(+) allogeneic T cells compared with untreated B cells and B cells treated with CT-B and LTK63. Finally, only treatment with toxins or FSK induced antigen-specific T-cell proliferation in Mycobacterium tuberculosis purified protein derivative or tetanus toxoid responder donors. Taken together, these results indicated that the in vitro effects of CT and LT on human B cells are mediated by cAMP.
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