The Mechanism of Superantigen-Mediated Toxic Shock: Not a Simple Th1 Cytokine Storm
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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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In mouse models of toxic shock, TNF is the cytokine driver of superantigen-driven cytokine storm.
“In mouse models of toxic shock, TNF is the cytokine driver of superantigen-driven cytokine storm.”
From Cytokine storm (2020) · cites this paper as [39]
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- Authors
- Faulkner, L., Cooper, A., Fantino, C., Altmann, D. M., & Sriskandan, S.
- Affiliations
- Imperial College London (GB)
- 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
- 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
- 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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