ArticleInfection and immunity2007
Staphylococcal enterotoxin B in vivo modulates both gamma interferon receptor expression and ligand-induced activation of signal transducer and activator of transcription 1 in T cells.
Article in Infection and immunity, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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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Who cites it
7 citing papers in PubMed, 20 citations in OpenAlex.
- Novel insights into the immune response to bacterial T cell superantigens.Nature reviews. Immunology · 2024Review
- Manipulation of Innate and Adaptive Immunity by Staphylococcal Superantigens.Pathogens (Basel, Switzerland) · 2018Review
- MHC Class II Activation and Interferon-γ Mediate the Inhibition of Neutrophils and Eosinophils by Staphylococcal Enterotoxin Type A (SEA).Frontiers in cellular and infection microbiology · 2017Article
- Staphylococcal enterotoxin B-induced microRNA-155 targets SOCS1 to promote acute inflammatory lung injury.Infection and immunity · 2014Article
- Late multiple organ surge in interferon-regulated target genes characterizes staphylococcal enterotoxin B lethality.PloS one · 2014Article
- Relationship of varying patterns of cytokine production to the anorexic and neuroendocrine effects of repeated Staphylococcal enterotoxin A exposure.Journal of neuroimmunology · 2008Article
- Activation of STAT6 by intranasal allergens correlated with the development of eosinophilic chronic rhinosinusitis in a mouse model.International journal of immunopathology and pharmacologyArticle
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Superantigens (SAg) are bacterial exotoxins that provoke extreme responses in the immune system; for example, the acute hyperactivation of SAg-reactive T cells that leads to toxic shock syndrome is followed within days by strong immunosuppression. The gamma interferon (IFN-gamma) response is deeply affected in both extremes. The implication of IFN-gamma in the pathophysiology of lethal shock induced in mice after a secondary challenge with the SAg staphylococcal enterotoxin B (SEB) prompted us to study the regulation of IFN-gamma secretion and the intracellular response. We demonstrate in this study that a rechallenge with SEB becomes lethal only when given inside a critical time window after SEB priming and is associated with an increase of IFN-gamma serum release 72 h after priming. However, at this time, a selective blockade of IFN-gamma/STAT1 signaling develops in spleen cells, correlating with a lack of expression of the IFN-gamma receptor beta subunit and STAT1 in the T-cell population. Selective blockade of the STAT1 signaling pathway--while simultaneously maintaining STAT3 signaling and expression--may be a protective mechanism that shortens IFN-gamma production during the Th1 effector response. This blockade may also have consequences on switching towards a suppressor phenotype with chronic exposure to the superantigen.
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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.