Contribution of Malassezia spp. to the development of atopic dermatitis

The prevalence of atopic dermatitis (AD) has been increasing. Whereas AD symptoms are obvious and easy to recognise, the etiopathogenesis remains not fully elucidated. Recently, the role of microorganisms and their impact on the immunology of AD have been discussed. In this review, we summarise a possible role of Malassezia in the development and persistence of eczema in patients with atopic eczema/dermatitis syndrome. A high proportion of AD patients present with a positive reaction to Malassezia allergens. Several possible pathogenic mechanisms enable Malassezia to trigger the development of AD. Malassezia spp. may release more allergens in a less acidic (pH <6), typical for AD, environment. The similarity between fungal thioredoxin and human proteins causes T-cell cross-reactivity. TLR-mediated mechanisms are involved in host response against Malassezia spp. An interaction between Malassezia spp. and keratinocytes alters the profile of cytokine release, and what is more, yeast cells can survive when absorbed by keratinocytes. Dendritic cells of AD patients induced by Malassezia are less susceptible to lysis mediated by NK cells which exerts a pro-inflammatory effect. Despite the evidence that Malassezia spp. contribute to the development of AD, the pathogenetic mechanisms and relationship between Malassezia and immune defense remain partly unexplained and require further research.