ArticleProceedings of the National Academy of Sciences of the United States of America1996
Differential effects of staphylococcal toxic shock syndrome toxin-1 on B cell apoptosis.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 52 citations in OpenAlex.
- The Role ofInternational journal of molecular sciences · 2022Review
- Superantigens and SARS-CoV-2.Pathogens (Basel, Switzerland) · 2022Article
- Safety and Immunogenicity of a 4-Component Toxoid-BasedFrontiers in immunology · 2021Article
- Selective Host Cell Death byFrontiers in immunology · 2020Review
- TBAScientific reports · 2019Article
- Nasopharyngeal infection byProceedings of the National Academy of Sciences of the United States of America · 2017Article
- Superantigens Modulate Bacterial Density during Staphylococcus aureus Nasal Colonization.Toxins · 2015Article
- The staphylococcal enterotoxin (SE) family: SEB and siblings.Virulence · 2013Review
- A new pathway of staphylococcal pathogenesis: apoptosis-like death induced by Staphopain B in human neutrophils and monocytes.Journal of innate immunity · 2009Article
- More than one tandem repeat domain of the extracellular adherence protein of Staphylococcus aureus is required for aggregation, adherence, and host cell invasion but not for leukocyte activation.Infection and immunity · 2008Article
- Regulation of Apoptosis by Gram-Positive Bacteria: Mechanistic Diversity and Consequences for Immunity.Current immunology reviews · 2006Article
- The effect of site-specific monoclonal antibodies directed to toxic shock syndrome toxin-1 in experimental Staphylococcus aureus arthritis.Clinical and experimental immunology · 1999Article
- T cell- and perforin-dependent depletion of B cells in vivo by staphylococcal enterotoxin A.Immunology · 1998Article
- Acylation of Escherichia coli hemolysin: a unique protein lipidation mechanism underlying toxin function.Microbiology and molecular biology reviews : MMBR · 1998Review
- Perspectives series: host/pathogen interactions. Apoptosis in bacterial pathogenesis.The Journal of clinical investigation · 1997Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Superantigens, such as toxic shock syndrome toxin 1 (TSST-1), have been implicated in the pathogenesis of several autoimmune and allergic diseases associated with polyclonal B cell activation. In this report, we studied the in vitro effects of TSST-1 on B cell activation. We show herein that TSST-1 produced antagonistic effects on Ig synthesis by peripheral blood mononuclear cells (PBMC) from normal subjects, depending on the concentration used; Ig production was inhibited at 1000 pg/ml (P < 0.01) and enhanced at 1 and 0.01 pg/ml (P < 0.01) of toxin. Cultures of PBMC were then examined for morphologic features and DNA fragmentation characteristic for apoptosis. B cells exhibited a significantly higher (P < 0.01) incidence of apoptosis after stimulation with 1000 pg/ml of TSST-1 compared with 1 or 0.01 pg/ml of toxin or medium alone. Abundant expression of Fas, a cell surface protein that mediates apoptosis, was detected on B cells after stimulation with 1000 pg/ml of TSST-1 and was significantly higher on B cells undergoing apoptosis than on live cells (P = 0.01). Additionally, increased Fas expression and B cell death occurred at concentrations of TSST-1 inducing the production of high amounts of gamma interferon (IFN-gamma), and both events could be blocked by neutralizing anti-IFN-gamma antibody. These findings suggest that high concentrations of TSST-1 can induce IFN-gamma-dependent B cell apoptosis, whereas at low concentrations it stimulates Ig synthesis by PBMC from normal subjects. These findings support the concept that staphylococcal toxins have a role in B cell hyperactivity in autoimmunity and allergy.
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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.