학술논문

The allergic march from Staphylococcus aureus superantigens to immunoglobulin E.
Document Type
Academic Journal
Author
Gould HJ; Divisions of Cell and Molecular Biophysics and Allergy, Asthma and Lung Biology, and MRC and Asthma UK Centre in Allergic Mechanisms of Asthma, King's College London, UK.; Takhar PHarries HEChevretton ESutton BJ
Source
Publisher: Karger Country of Publication: Switzerland NLM ID: 101183835 Publication Model: Print Cited Medium: Print ISSN: 1660-2242 (Print) Linking ISSN: 00796034 NLM ISO Abbreviation: Chem Immunol Allergy Subsets: MEDLINE
Subject
Language
English
ISSN
1660-2242
Abstract
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.