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

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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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Authors: Faulkner, L., Cooper, A., Fantino, C., Altmann, D. M., & Sriskandan, S.
Affiliations: Imperial College London (GB)
ORCID: Faulkner, Lee
Altmann, Daniel M
Sriskandan, Shiranee
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: bronze
doi.org
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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The Mechanism of Superantigen-Mediated Toxic Shock: Not a Simple Th1 Cytokine Storm

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