Abstract
The currently accepted model for superantigen (SAg) induced T cell activation suggests that SAg, without being processed, cross link both MHC class II, from Antigen Presenting Cells (APC), and V-β , from T-cell receptor (TCR), initi-ating 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 discov-ered 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 Staphy-lococcal enterotoxin A (SEA) to itself or neigh- boring CD4+ T cells via MHC class II, thus in-ducing massive CD4+ T cell proliferation. Treat- ment with neutralizing anti MHC class II anti-body inhibits this CD4+ T cell proliferation re-sponse. The fact that murine CD4+ T cells ex-press MHC class II offers new insight about SAg activity. Based on our findings, we propose re-vising and extending previous models for SAg induced T cell activation, altering previous models of MHC class II restriction of T cell re-sponses to SEA as well as the requirement for SAg processing.
Highlights
Staphylococcus aureus is a major bacterial pathogen causing several diseases including food-borne illnesses [1]
Our hypothesis is that the ratio between antigen presenting cell (APC) and T cell is important for efficient T-cell proliferation, and that there would be a reduction in CD4+ T-Cell proliferation response after altering this ratio, because reduction in APCs limits the number of CD4+ T cells that can bind to the Staphylococcal enterotoxin A (SEA)-APC complex
Our studies demonstrate for the first time a subtype of mouse naïve CD4+ T cells express MHC class II molecules on the cell surface
Summary
Staphylococcus aureus is a major bacterial pathogen causing several diseases including food-borne illnesses [1]. SAg plays an important role in pathogenesis by undermining the specificity of the adaptive immune response They are reported to be associated with etiology of several human diseases including toxic shock syndrome, Kawasaki disease, guttate psoriasis, eczema, rheumatoid arthritis and scarlet fever [4]. The current model for superantigen activity suggests that native, unprocessed SAg bind directly to the helical chain of the MHC class II, outside the peptide binding groove of the antigen presenting cell (APC) [5]. This binding takes place without proteolytic degradation and fragmentation, internalization, and re-expression of the SAg degraded short fragments on the cell surface. The currently accepted model, suggests that both types of cells; APC and T cells, are needed for SAg induced T-cell proliferation [7,8]
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