FcεRIα, encoded by the FCER1A gene, is the α -subunit of the high-affinity receptor for the Fc portion of immunoglobulin E (IgE). It plays a central role in IgE-mediated allergic disorders, as well as in the immunity and immunopathology of some parasitic infections. FcεRIα is specifically expressed on basophils and mast cells, and its expression is known to be promoted by the IL-3-GATA-2 pathway during cell differentiation [2].

In atopic dermatitis (AD), lesional AD samples are characterized by the expansion of inflammatory dendritic cells (CD1A + FCER1A +), suggesting a role of FCER1A-expressing cells in the disease [1]. Mice deficient in FCER1A-AS, a co-expressed natural antisense RNA of FCER1A, demonstrated a similar phenotype to FCER1A knockout mice in Schistosoma japonicum infection and in IgE-FcεRIα-mediated cutaneous anaphylaxis. This indicates that FCER1A-AS is essential for the expression of FCER1A-S mRNA and proteins, and thus for IgE-dependent immunity [2].

In conclusion, FCER1A is crucial for IgE-mediated immune responses. Studies using gene-deficient mouse models, such as those lacking FCER1A-AS which mimics FCER1A knockout, have revealed its role in allergic and anti-parasitic immune responses. These findings contribute to our understanding of diseases like atopic dermatitis and IgE-mediated anaphylaxis, providing insights that may help in developing new treatment strategies.