Atopic dermatitis is a complex disease in which a strong interaction between alterations of skin barrier and the
adaptive immune system coexists. In the recent years, new findings have underlined the importance of skin proteins,
especially filaggrin, which participate to the outmost layers of the skin. To strengthen this physical barrier, many factors
are available, such as antimicrobial peptides, chemokines and cytokines produced by keratinocytes. Skin disruption can
easily allow the allergen penetration and the local keratinocytes can promote the adaptive immune response toward a Th2
phenotype. On the other side, allergic Th2 cytokines may downregulate the production of skin barrier proteins, facilitating
the penetration of allergens. Moreover, data on murine models show the absolute relevance of the systemic immune
system to develop clinical skin reaction. Since the clinical aspect of patients with AD does not show different patterns
whatever is the prevalent underlying mechanism, in clinical practice it is difficult to translate the different endotypes
beside the IgE and non IgE associated forms. The aim of this review is to point out to the most recent knowledge in this
field, which makes AD more difficult to frame in a unique clinical entity.
Immune Alterations in IgE and Non IgE-Associated Atopic Dermatitis