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The toxicity of staphylococcal enterotoxin B in mice is mediated by T cells
P Marrack1, M Blackman, E Kushnir
1Howard Hughes Medical Institute, Department of Medicine, National Jewish Center for Immunology and Respiratory Medicine, Denver, Colorado 80206.
Abstract:
Staphylococcal enterotoxin B (SEB) has been shown in the past to be a potent T cell stimulant in mouse or man. The toxin acts as a superantigen that is, it binds to class II MHC proteins and, as such a complex, stimulates T cells bearing particular V beta s as part of their receptors. The toxin also has several pathological effects, causing, in mice, rapid weight loss, thymus atrophy, immunosuppression, and, at high doses, death. The data in this paper show that at least one of these effects, weight loss, is T cell mediated. Staphylococcal enterotoxin-mediated weight loss is MHC dependent, and is almost absent in animals expressing MHC class II molecules, which, complexed with SEB, are poor T cell stimulants. Also, mice that lack T cell function, genetically or because of cyclosporin A treatment, lose no or less weight than controls in response to SEB. Finally, animals bred such that they express few T cells bearing V beta s with which SEB can interact lose much less weight in response to the toxin than littermate controls that have higher numbers of reactive T cells. It is therefore suggested that the pathological effects of the staphylococcal, T cell-stimulating toxins in mouse and man may be partially or wholly the consequence of massive T cell stimulation.
Insights
Staphylococcal enterotoxin B (SEB) causes weight loss in mice, mediated by T cells. This effect is dependent on MHC class II molecules and T cell receptor interactions, highlighting T cell stimulation
Area of Science:
- Immunology
- Microbiology
Background:
- Staphylococcal enterotoxin B (SEB) is a potent T cell stimulant and superantigen.
- SEB causes pathological effects in mice, including weight loss and thymus atrophy.
Purpose of the Study:
- To determine if SEB-induced weight loss is T cell-mediated.
- To investigate the role of MHC class II and T cell receptor interactions in SEB-induced pathology.
Main Methods:
- Administering SEB to mice with varying T cell function and MHC expression.
- Utilizing genetic modification and cyclosporin A treatment to modulate T cell activity.
- Comparing weight loss in response to SEB across different mouse models.
Main Results:
- SEB-induced weight loss is significantly reduced in T cell-deficient mice.
- Mice lacking functional MHC class II molecules exhibit minimal weight loss.
- Mice with limited T cell receptor V beta expression show reduced susceptibility to SEB-induced weight loss.
Conclusions:
- SEB-induced weight loss is a T cell-mediated phenomenon.
- The pathological effects of SEB are linked to massive T cell stimulation via superantigen activity.