ArticleThe Journal of experimental medicine2005
Anthrax toxins suppress T lymphocyte activation by disrupting antigen receptor signaling.
Article in The Journal of experimental medicine, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 86 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
86 citing papers in PubMed, 161 citations in OpenAlex.
- Clostridioides difficile toxin B subverts germinal center and antibody recall responses by stimulating a drug-treatable CXCR4-dependent mechanism.Cell reports · 2024Article
- Dachshund Homolog 1: Unveiling Its Potential Role in Megakaryopoiesis andInternational journal of molecular sciences · 2024Article
- Systematic and Comprehensive Analysis of tRNA-Derived Small RNAs Reveals Their Potential Regulatory Roles and Clinical Relevance in Sarcoidosis.Journal of inflammation research · 2023Article
- Bacterial Nucleotidyl Cyclases Activated by Calmodulin or Actin in Host Cells: Enzyme Specificities and Cytotoxicity Mechanisms Identified to Date.International journal of molecular sciences · 2022Review
- The Immunological Synapse: An Emerging Target for Immune Evasion by Bacterial Pathogens.Frontiers in immunology · 2022Review
- Multiple stages of evolutionary change in anthrax toxin receptor expression in humans.Nature communications · 2021Article
- CARD8 inflammasome activation triggers pyroptosis in human T cells.The EMBO journal · 2020Article
- Current Status and Trends in Prophylaxis and Management of Anthrax Disease.Pathogens (Basel, Switzerland) · 2020Review
- Rapid Discovery and Characterization of Synthetic Neutralizing Antibodies against Anthrax Edema Toxin.Biochemistry · 2019Article
- Article
- A Bivalent Protein r-PAbxpB Comprising PA Domain IV and Exosporium Protein BxpB Confers Protection AgainstFrontiers in immunology · 2019Article
- A bivalent protein r-PB, comprising PA and BclA immunodominant regions for comprehensive protection against Bacillus anthracis.Scientific reports · 2018Article
- Compartmentalized Cyclic AMP Production by theFrontiers in immunology · 2018Article
- Anthrax Vaccine Precipitated Induces Edema Toxin-Neutralizing, Edema Factor-Specific Antibodies in Human Recipients.Clinical and vaccine immunology : CVI · 2017Article
- HDAC8 Prevents Anthrax Lethal Toxin-induced Cell Cycle Arrest through Silencing PTEN in Human Monocytic THP-1 Cells.Toxins · 2017Article
- The Molecular Basis of Toxins' Interactions with Intracellular Signaling via Discrete Portals.Toxins · 2017Review
- Article
- Tumor Targeting and Drug Delivery by Anthrax Toxin.Toxins · 2016Review
- Article
- Micropatterned macrophage analysis reveals global cytoskeleton constraints induced by Bacillus anthracis edema toxin.Infection and immunity · 2015Article
26 more citing papers are in PubMed but not listed here.
Corrections and comments
- Commented on by
Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Anthrax is an infection caused by pathogenic strains of Bacillus anthracis, which secretes a three-component toxic complex consisting of protective antigen (PA), edema factor (EF), and lethal factor (LF). PA forms binary complexes with either LF or EF and mediates their entry into host cells. Although the initial phases of bacterial growth occur in the lymph node, the host fails to mount an effective immune response. Here, we show that LT and ET are potent suppressors of human T cell activation and proliferation triggered through the antigen receptor. Both LT and ET inhibit the mitogen-activated protein and stress kinase pathways, and both toxins inhibit activation of NFAT and AP-1, two transcription factors essential for cytokine gene expression. These data identify a novel strategy of immune evasion by B. anthracis, based on both effector subunits of the toxic complex, and targeted to a key cellular component of adaptive immunity.
Indexed as
Identifiers
What OpenQuestion holds
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.