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PI3K/Akt/mTOR, a pathway less recognized for staphylococcal superantigen-induced toxicity
1Department of Immunology, Integrated Toxicology Division, United States Army Medical Research Institute of Infectious Diseases, Fort Detrick, Frederick, MD 21702, USA. teresa.krakauer@us.army.mil
Toxins
|December 4, 2012
Summary
Staphylococcal enterotoxin B (SEB) superantigens activate immune cells, causing disease. This review details SEB
Area of Science:
- Immunology
- Toxicology
- Molecular Biology
Background:
- Staphylococcal enterotoxin B (SEB) and related superantigens are potent immune activators.
- These toxins induce T-cell and monocyte/macrophage hyperactivation via MHC class II and TCR interactions.
- SEB-induced toxicity manifests as fever, hypotension, and shock due to excessive cytokine release.
Purpose of the Study:
- To review signaling molecules involved in superantigen-induced toxicity.
- To update potential therapeutics targeting superantigens.
Main Methods:
- Review of signal transduction pathways.
- Analysis of PI3K/Akt/mTOR pathway activation by superantigens.
Main Results:
- SEB activates MAPK and cytokine receptor signaling pathways, leading to NF-κB activation.
- IL-2, IFN-γ, and chemokines activate PI3K/Akt/mTOR pathways.
- These pathways culminate in staphylococcal superantigen-induced toxicity.
Conclusions:
- Understanding SEB-induced signaling is crucial for developing effective therapeutics.
- Targeting PI3K/Akt/mTOR pathways offers potential therapeutic strategies against superantigens.
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