Abstract

Malassezia yeasts are implicated in the pathogenesis of two common diseases: seborrheic and atopic eczema. Seborrheic eczema (SE) affects areas of the body with an increased density of sebaceous glands (scalp, mid eyebrow, nasolabial folds, sternum and interscapular regions) and body folds). M. globosa and M. restricta are more commonly isolated in lesional skin, but this is also true for the isolation rate from healthy skin. In lesions of SE, a nonimmunogenic irritant reaction is recognized by immunocytochemistry. SE-specific molecular subtypes of M. globosa, M. restricta, and M. furfur have been recognized. Production of potent aryl hydrocarbon receptor ligands by Malassezia yeasts could offer new insight in the pathogenesis of SE through modulation of the immune system. The persistent and recurring nature of SE is highlighted through the existence of multiple, but not yet curative topical and systemic therapies. Atopic eczema (AE) has variable clinical presentation of skin lesions depending on the age of the patient. Three types of AE are recognized: “extrinsic,” “intrinsic,” and one-third group of patients with extrinsic or intrinsic AE showing IgE-mediated sensitization to self-antigens. Malassezia yeasts have been shown to act as allergens in AE, and thirteen allergens have been cloned, characterized, and produced as recombinant proteins from Malassezia species. Some of these recombinant allergens show a high degree of sequence identity to homologous human self antigens. The human proteins are capable of inducing positive skin prick and atopy patch tests in patients sensitized to the Malassezia proteins, indicating a role of IgE-mediated autoreactivity in the pathogenesis of AE in a subset of patients. The recombinant allergens will contribute to improve the diagnosis of sensitization to the yeast in AE patients. A correct patient stratification according to specific sensitization patterns could open novel possibilities for an immunotherapeutic treatment of a subset of AE patients in the future.

Full Text
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