The allergic march from Staphylococcus aureus superantigens to immunoglobulin E

Staphylococcus aureus is a commensal bacterium in the respiratory tract mucosa of most people and infects the skin of atopic dermatitis patients. This might imply a symbiotic relationship between host and bacterium or a standoff between bacterial infection and the host immune system. But superantigens produced by S. aureus in these locations are of particular interest because they are strongly implicated in the pathogenesis of allergic disorders and airway disease. They appear to act locally in these conditions by stimulating polyclonal T cell and B cell proliferation and driving somatic hypermutation, class switching to immunoglobulin (Ig) E and the production of allergen-specific IgE in mucosal B cells. IgE antibodies directed against the superantigens ('superallergens') themselves engender chronic inflammation and the persistent sensitization to conventional allergens of mast cells and antigen-presenting cells in mucosal tissues in atopic dermatitis, rhinitis and asthma. Moreover, S. aureus superantigens inhibit the activity of T regulatory cells that normally control inflammation, and generate a state of steroid resistance that confounds treatment of allergic disorders and airway disease.