ArticleThe Journal of experimental medicine2014
B lymphocytes undergo TLR2-dependent apoptosis upon Shigella infection.
Article in The Journal of experimental medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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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.
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Who cites it
31 citing papers in PubMed, 58 citations in OpenAlex.
- Review
- Shigellosis.Lancet (London, England) · 2025Review
- Shigella sonnei: epidemiology, evolution, pathogenesis, resistance and host interactions.Nature reviews. Microbiology · 2025Review
- Cell Death and Infection: Implications for Host and Microbe.Advances in experimental medicine and biology · 2025Review
- Mapping the functional B-cell epitopes ofApplied and environmental microbiology · 2024Article
- Article
- Ascorbate deficiency increases progression of shigellosis in guinea pigs and mice infection models.Gut microbes · 2023Article
- Molecular mechanisms of Shigella effector proteins: a common pathogen among diarrheic pediatric population.Molecular and cellular pediatrics · 2022Review
- TheMicroorganisms · 2021Review
- The Intriguing Interaction of Escherichia coli with the Host Environment and Innovative Strategies To Interfere with Colonization: a Summary of the 2019 E. coli and the Mucosal Immune System Meeting.Applied and environmental microbiology · 2020Article
- Shigella impairs human T lymphocyte responsiveness by hijacking actin cytoskeleton dynamics and T cell receptor vesicular trafficking.Cellular microbiology · 2020Article
- Bacteria That Cause Enteric Diseases Stimulate Distinct Humoral Immune Responses.Frontiers in immunology · 2020Review
- Review
- Human Intestinal Enteroids as a Model System ofInfection and immunity · 2019Article
- Review
- Review
- Role of a fluid-phase PRR in fighting an intracellular pathogen: PTX3 in Shigella infection.PLoS pathogens · 2018Article
- Recent insights into Shigella.Current opinion in infectious diseases · 2018Review
- HrpE, the major component of the Xanthomonas type three protein secretion pilus, elicits plant immunity responses.Scientific reports · 2018Article
- Injection of T3SS effectors not resulting in invasion is the main targeting mechanism ofProceedings of the National Academy of Sciences of the United States of America · 2017Article
Corrections and comments
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Authors and funding
12 authors at 6 institutions in 3 countries.
Funding
Abstract
Antibody-mediated immunity to Shigella, the causative agent of bacillary dysentery, requires several episodes of infection to get primed and is short-lasting, suggesting that the B cell response is functionally impaired. We show that upon ex vivo infection of human colonic tissue, invasive S. flexneri interacts with and occasionally invades B lymphocytes. The induction of a type three secretion apparatus (T3SA)-dependent B cell death is observed in the human CL-01 B cell line in vitro, as well as in mouse B lymphocytes in vivo. In addition to cell death occurring in Shigella-invaded CL-01 B lymphocytes, we provide evidence that the T3SA needle tip protein IpaD can induce cell death in noninvaded cells. IpaD binds to and induces B cell apoptosis via TLR2, a signaling receptor thus far considered to result in activation of B lymphocytes. The presence of bacterial co-signals is required to sensitize B cells to apoptosis and to up-regulate tlr2, thus enhancing IpaD binding. Apoptotic B lymphocytes in contact with Shigella-IpaD are detected in rectal biopsies of infected individuals. This study therefore adds direct B lymphocyte targeting to the diversity of mechanisms used by Shigella to dampen the host immune response.
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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.