Submitted to: Open Journal of Immunology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: June 20, 2011
Publication Date: June 30, 2011
Citation: Rasooly, R., Do, P.M., Hernlem, B.J. 2011. Auto-presentation of Staphylococcal enterotoxin A by mouse CD4+ T cells. Open Journal of Immunology. 1(1):8-14. doi:10.4236/oji.2011.11002. Interpretive Summary: Staphylococcal enterotoxins (SEs) produced by pathogenic bacteria Staphylococcus aureus cause food poisoning and act as a superantigen (SAg), causing massive activation and proliferation of T-cells and cytokine release. Massive cytokines releases are associated with several human diseases. This paper suggest that the safety mechanism requiring interaction between two different types of cells do not occur as a response to SAg; consequently inducing nonspecific T cell over-activation with massive cytokine release. This paper demonstrates that SAg induced T cell activation may require only one type of cell performing the role of both Antigen Presenting Cells and T-cell receptor. The described new observations and interpretation of the experimental data offer further insight into the mechanism that governs adverse effects of staphylococcus enterotoxins.
Technical Abstract: The currently accepted model for superantigen (SAg )induced T cell activation suggests that SAg, without being processed, cross links both MHC class II, from Antigen Presenting Cells (APC), and V-beta, from T-cell receptor (TCR), initiating nonspecific T-cell activation. This T-cell proliferation induces a massive cytokine release associated with several human diseases. It is thought that murine CD4+ T cells do not express MHC class-II molecules. However, we discovered that a subtype of mouse naïve CD4+ T cells expresses MHC class II on their cell surface and that these CD4+ T cells can perform the role of both APC and T cells, able to present Staphylococcal enterotoxin A (SEA) to itself or neighboring CD4+ T cells via MHC class II, thus inducing massive CD4+ T cell proliferation. Treatment with neutralizing anti MHC class II antibody inhibits this CD4+ T cell proliferation response. The fact that murine CD4+ T cells express MHC class II offers new insight about SAg activity. Based on our findings, we propose revising and extending previous models for SAg induced T cell activation, altering previous models of MHC class II restriction of T cell responses to SEA as well as the requirement for SAg processing.