ArticleProceedings of the National Academy of Sciences of the United States of America2013
Shigella impairs T lymphocyte dynamics in vivo.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 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.
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Who cites it
32 citing papers in PubMed, 46 citations in OpenAlex.
- Multifunctional antibody responses from a primateScience translational medicine · 2026Article
- Protective and pathogenic antibody responses from a primate Shigella outbreak inform vaccine design.bioRxiv : the preprint server for biology · 2025Article
- Shigellosis.Lancet (London, England) · 2025Review
- Ascorbate deficiency increases progression of shigellosis in guinea pigs and mice infection models.Gut microbes · 2023Article
- Mechanical Forces Govern Interactions of Host Cells with Intracellular Bacterial Pathogens.Microbiology and molecular biology reviews : MMBR · 2022Review
- Microbiota-Host-Irinotecan Axis: A New Insight Toward Irinotecan Chemotherapy.Frontiers in cellular and infection microbiology · 2021Review
- T Cell Immunity to Bacterial Pathogens: Mechanisms of Immune Control and Bacterial Evasion.International journal of molecular sciences · 2020Review
- Shigella impairs human T lymphocyte responsiveness by hijacking actin cytoskeleton dynamics and T cell receptor vesicular trafficking.Cellular microbiology · 2020Article
- Cytosolic Gram-negative bacteria prevent apoptosis by inhibition of effector caspases through lipopolysaccharide.Nature microbiology · 2020Article
- Bacteria That Cause Enteric Diseases Stimulate Distinct Humoral Immune Responses.Frontiers in immunology · 2020Review
- Review
- Review
- Regulated DelayedTheranostics · 2019Article
- Review
- Recent insights into Shigella.Current opinion in infectious diseases · 2018Review
- Direct Manipulation of T Lymphocytes by Proteins of Gastrointestinal Bacterial Pathogens.Infection and immunity · 2018Review
- A Model of Superinfection of Virus-Infected Zebrafish Larvae: Increased Susceptibility to Bacteria Associated With Neutrophil Death.Frontiers in immunology · 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
- Biosafety Level 3 setup for multiphoton microscopy in vivo.Scientific reports · 2017Article
- How Do the Virulence Factors ofFrontiers in cellular and infection microbiology · 2017Review
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Authors and funding
10 authors at 5 institutions in 3 countries.
Funding
Abstract
The Gram-negative enteroinvasive bacterium Shigella flexneri is responsible for the endemic form of bacillary dysentery, an acute rectocolitis in humans. S. flexneri uses a type III secretion system to inject effector proteins into host cells, thus diverting cellular functions to its own benefit. Protective immunity to reinfection requires several rounds of infection to be elicited and is short-lasting, suggesting that S. flexneri interferes with the priming of specific immunity. Considering the key role played by T-lymphocyte trafficking in priming of adaptive immunity, we investigated the impact of S. flexneri on T-cell dynamics in vivo. By using two-photon microscopy to visualize bacterium-T-cell cross-talks in the lymph nodes, where the adaptive immunity is initiated, we provide evidence that S. flexneri, via its type III secretion system, impairs the migration pattern of CD4(+) T cells independently of cognate recognition of bacterial antigens. We show that bacterial invasion of CD4(+) T lymphocytes occurs in vivo, and results in cell migration arrest. In the absence of invasion, CD4(+) T-cell migration parameters are also dramatically altered. Signals resulting from S. flexneri interactions with subcapsular sinus macrophages and dendritic cells, and recruitment of polymorphonuclear cells are likely to contribute to this phenomenon. These findings indicate that S. flexneri targets T lymphocytes in vivo and highlight the role of type III effector secretion in modulating host adaptive immune responses.
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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.