No abstract

Atopic dermatitis (AD) is a chronic inflammatory skin disease caused by skin barrier dysfunction and dysregulated immune responses. Mast cells (MCs) reportedly contribute to IgE-mediated diseases including AD, and play a key role in the pathogenesis of AD. Unlike the classical IgE-mediated mechanism, nearly half of children have no increase in serum IgE, and avoidance of sensitizing substances does not prevent skin lesions. Mas-related G protein coupled receptor X2 (MrgprX2) is a MC membrane receptor and the homologous gene in mouse is MrgprB2. Recently, MrgprX2(B2) has been reported to selectively and highly express on MCs and as an IgE-independent receptor to activate MCs. However, the role of MrgprX2(B2) in AD still remains unclear. Here we collected AD patients' skin and induced acute AD-like skin lesions in BALB/c mice, we found that the expression of MrgprX2(B2) is upregulated in AD skin lesions by using immunofluorescence, real time PCR and flowcytometry. Collectively, these results demonstrate that MrgprX2(B2) may be involved in the IgEindependent mast cell activation in AD.