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Cited by 122T-cell and B-cell ImmunologyImmune Response and InflammationAntimicrobial Resistance in Staphylococcus

The DOI matches its Crossref record; 51 of the 51 references it cites were found in a registry or an index.

The Mechanism of Superantigen-Mediated Toxic Shock: Not a Simple Th1 Cytokine Storm

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Faulkner, Lee, Cooper, Anneli, Fantino, Cristina, Altmann, Daniel M, Sriskandan, Shiranee·2005·The Journal of Immunology
DOI 10.4049/jimmunol.175.10.6870
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Abstract

The profound clinical consequences of Gram-positive toxic shock are hypothesized to stem from excessive Th1 responses to superantigens. We used a new superantigen-sensitive transgenic model to explore the role of TCRαβ T cells in responses to staphylococcal enterotoxin B (SEB) in vitro and in two different in vivo models. The proliferative and cytokine responses of HLA-DR1 spleen cells were 100-fold more sensitive than controls and were entirely dependent on TCRαβ T cells. HLA-DR1 mice showed greater sensitivity in vivo to two doses of SEB with higher mortality and serum cytokines than controls. When d-galactosamine was used as a sensitizing agent with a single dose of SEB, HLA-DR1 mice died of toxic shock whereas controls did not. In this sensitized model of toxic shock there was a biphasic release of cytokines, including TNF-α, at 2 h and before death at 7 h. In both models, mortality and cytokine release at both time points were dependent on TCRαβ T cells. Anti-TNF-α pretreatment was protective against shock whereas anti-IFN γ pretreatment and delayed anti-TNF-α treatment were not. Importantly, anti-TNF-α pretreatment inhibited the early TNF-α response but did not inhibit the later TNF-α burst, to which mortality has previously been attributed. Splenic T cells were shown definitively to be the major source of TNF-α during the acute cytokine response. Our results demonstrate unequivocally that TCRαβ T cells are critical for lethality in toxic shock but it is the early TNF-α response and not the later cytokine surge that mediates lethal shock.

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Metadata

Authors
Faulkner, L., Cooper, A., Fantino, C., Altmann, D. M., & Sriskandan, S.
Affiliations
Imperial College London (GB)
ORCID
Venue
The Journal of Immunology
Publisher
Oxford University Press (OUP)
Published
2005-11
Volume
175
Issue
10
Pages
6870-6877
ISSN
  • 0022-1767 (ISSN-L)
  • 1550-6606
DOI
10.4049/jimmunol.175.10.6870
OpenAlex
W2111438490
Cited by
122
References
51
Citations by year
2026: 3 · 2025: 5 · 2024: 4 · 2023: 6 · 2022: 7 · 2021: 7 · 2020: 9 · 2019: 7 · 2018: 5 · 2017: 6 · 2016: 2 · 2015: 5 · 2014: 7 · 2013: 6 · 2012: 5
FWCI
2.35
Type
journal article
Language
en
Open access
Licence
academic.oup.com/pages/standard-publication-reuse-rights (vor)
Locations
  • The Journal of Immunology (publishedVersion)
  • PubMed (publishedVersion)
  • ENLIGHTEN (Jurnal Bimbingan dan Konseling Islam) (submittedVersion)
Topics
  • Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
  • Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
  • Health Sciences › Medicine › Infectious Diseases › Antimicrobial Resistance in Staphylococcus
Keywords
staphylococcal enterotoxin B, TNF-α, cytokine storm, Th1 response, D-galactosamine sensitization, splenic T cells, interferon-gamma
MeSH terms
Animals, Enterotoxins, Galactosamine, Humans, Mice, Transgenic, Shock, Septic, Spleen, Tumor Necrosis Factor-alpha, HLA-DR1 Antigen, Cytokines, Receptors, Antigen, T-Cell, alpha-beta, Superantigens, Mice, Knockout, Th1 Cells, Mice

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