ArticleThe American journal of pathology2011
Human leukocyte antigen class II transgenic mouse model unmasks the significant extrahepatic pathology in toxic shock syndrome.
Article in The American journal of pathology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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.
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Who cites it
17 citing papers in PubMed, 26 citations in OpenAlex.
- IFN-American journal of respiratory cell and molecular biology · 2023Article
- Contribution of Staphylococcal Enterotoxin B to Staphylococcus aureus Systemic Infection.The Journal of infectious diseases · 2021Article
- "Small" Intestinal Immunopathology Plays a "Big" Role in Lethal Cytokine Release Syndrome, and Its Modulation by Interferon-γ, IL-17A, and a Janus Kinase Inhibitor.Frontiers in immunology · 2020Article
- Review
- Article
- Concomitant Disruption ofJournal of immunology (Baltimore, Md. : 1950) · 2017Article
- Rapid and Rigorous IL-17A Production by a Distinct Subpopulation of Effector Memory T Lymphocytes Constitutes a Novel Mechanism of Toxic Shock Syndrome Immunopathology.Journal of immunology (Baltimore, Md. : 1950) · 2017Article
- Staphylococcal Superantigens Spark Host-Mediated Danger Signals.Frontiers in immunology · 2016Review
- Superantigen-Producing Staphylococcus aureus Elicits Systemic Immune Activation in a Murine Wound Colonization Model.Toxins · 2015Article
- Superantigens produced by catheter-associated Staphylococcus aureus elicit systemic inflammatory disease in the absence of bacteremia.Journal of leukocyte biology · 2015Article
- Systemic inflammatory response elicited by superantigen destabilizes T regulatory cells, rendering them ineffective during toxic shock syndrome.Journal of immunology (Baltimore, Md. : 1950) · 2014Article
- The impact of Staphylococcus aureus-associated molecular patterns on staphylococcal superantigen-induced toxic shock syndrome and pneumonia.Mediators of inflammation · 2014Article
- Update on staphylococcal superantigen-induced signaling pathways and therapeutic interventions.Toxins · 2013Review
- Linezolid is superior to vancomycin in experimental pneumonia caused by Superantigen-Producing staphylococcus aureus in HLA class II transgenic mice.Antimicrobial agents and chemotherapy · 2012Article
- Chronic exposure to staphylococcal superantigen elicits a systemic inflammatory disease mimicking lupus.Journal of immunology (Baltimore, Md. : 1950) · 2012Article
- Staphylococcal superantigens in colonization and disease.Frontiers in cellular and infection microbiology · 2012Review
- Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Among the exotoxins produced by Staphylococcus aureus and Streptococcus pyogenes, the superantigens (SAgs) are the most potent T-cell activators known to date. SAgs are implicated in several serious diseases including toxic shock syndrome (TSS), Kawasaki disease, and sepsis. However, the immunopathogenesis of TSS and other diseases involving SAgs are still not completely understood. The commonly used conventional laboratory mouse strains do not respond robustly to SAgs in vivo. Therefore, they must be artificially rendered susceptible to TSS by using sensitizing agents such as d-galactosamine (d-galN), which skews the disease exclusively to the liver and, hence, is not representative of the disease in humans. SAg-induced TSS was characterized using transgenic mice expressing HLA class II molecules that are extremely susceptible to TSS without d-galN. HLA-DR3 transgenic mice recapitulated TSS in humans with extensive multiple-organ inflammation affecting the lung, liver, kidneys, heart, and small intestines. Heavy infiltration with T lymphocytes (both CD4(+) and CD8+), neutrophils, and macrophages was noted. In particular, the pathologic changes in the small intestines were extensive and accompanied by significantly altered absorptive functions of the enterocytes. In contrast to massive liver failure alone in the d-galN sensitization model of TSS, findings of the present study suggest that gut dysfunction might be a key pathogenic event that leads to high morbidity and mortality in humans with TSS.
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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.