Author(s): Cardona ID, Cho SH, Leung DY
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Abstract The role of staphylococcal superantigens in the pathophysiology of atopic dermatitis (AD) has been the focus of intense interest during the past decade. Although the increased prevalence of Staphylococcus aureus and its bacterial toxins in AD skin is well established, exploitation of the known mechanisms of superantigens in this disease for the development of novel therapies remains an active area of research. With the emergence of multi-drug resistant S. aureus, the need for a better understanding of the pathophysiology of bacterial superantigens in AD has become increasingly important. This review examines the mechanisms of S. aureus colonization and infection, of which the most important are defective skin barrier function, increased S. aureus adherence, and the decreased innate immune responses found in AD skin. The contribution of superantigens to the pathophysiology of AD is then discussed. Important immunologic mechanisms in this context include the role of superantigens in promoting T helper-2 skin inflammation, IgE production, T-regulatory cell subversion, expansion and migration of skin-homing T cells, and IgE anti-superantigen production. Lastly, these findings are discussed with reference to current therapeutic approaches, of which the most important include anti-inflammatory and antimicrobial medications, and future strategies, which are expected to consist of immune-modulators and synthetic antibacterials.
This article was published in Am J Clin Dermatol
and referenced in Journal of Clinical & Experimental Dermatology Research