ArticleCell reports2024
Clostridioides difficile toxin B subverts germinal center and antibody recall responses by stimulating a drug-treatable CXCR4-dependent mechanism.
Article in Cell reports, 2024. 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 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.
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Who cites it
8 citing papers in PubMed.
- The impact of TcdB conformational dynamics on vaccination against Clostridioides difficile.PLoS pathogens · 2026Article
- HumanbioRxiv : the preprint server for biology · 2025Article
- Immune Aspects of Clostridioides difficile Infection and Vaccine Development.Infectious disease clinics of North America · 2025Review
- Clostridioides difficile toxin A and toxin B inhibit toxin-specific adaptive immune responses through glucosyltransferase-dependent activity.Mucosal immunology · 2025Article
- The interplay between host immunity andmBio · 2025Review
- Enhanced immunogenicity of a Clostridioides difficile TcdB vaccine adjuvanted with a synthetic dual-TLR ligand adjuvant.NPJ vaccines · 2025Article
- A high-throughput chemotaxis assay for assessing immunotoxicity using multiple human immune cell types.NAM journal · 2025Article
- A multivalent mRNA-LNP vaccine protects againstScience (New York, N.Y.) · 2024Article
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
Recurrent Clostridioides difficile infection (CDI) results in significant morbidity and mortality. We previously established that CDI in mice does not protect against reinfection and is associated with poor pathogen-specific B cell memory (Bmem), recapitulating our observations with human Bmem. Here, we demonstrate that the secreted toxin TcdB2 is responsible for subversion of Bmem responses. TcdB2 from an endemic C. difficile strain delayed immunoglobulin G (IgG) class switch following vaccination, attenuated IgG recall to a vaccine booster, and prevented germinal center formation. The mechanism of TcdB2 action included increased B cell CXCR4 expression and responsiveness to its ligand CXCL12, accounting for altered cell migration and a failure of germinal center-dependent Bmem. These results were reproduced in a C. difficile infection model, and a US Food and Drug Administration (FDA)-approved CXCR4-blocking drug rescued germinal center formation. We therefore provide mechanistic insights into C. difficile-associated pathogenesis and illuminate a target for clinical intervention to limit recurrent disease.
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Registered trials
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