Atopy is characterized by a high production of IgE in response to common allergens exposure and by positive
responses to skin-prick test against specific antigens. Atopy can contribute to the development of atopic asthma and atopic
eczema. This condition involves the participation of different cells including mast cells that express the high-affinity Fc
receptor for IgE, the FcεRI receptor. Crosslinking of FcεRI-bound IgE in absence of an allergen increases the expression
of IgE receptor, enhances mast cells survival and induces synthesis and secretion of several inflammatory mediators that
contribute to increase allergic reactions. The number of mast cells and their mediators increase in asthma and eczema and
could be involved in the pathogenesis of these diseases.
Genetic factors such as mutations and polymorphism in several genes of the subunits of the FcεRI (receptor for IgE),
cytokines and their receptors (IL-4, IL-13), and transcription factors (STAT6) allow IgE synthesis. Moreover, epigenetic
regulation of genes such as DNA methylation and histone modifications are the genetic background of atopy.
This review attempts to summarize the recent progress on the pathology of atopy, its risk factors and the role of mast cells
in two atopic diseases: atopic asthma and atopic eczema.