Atopic dermatitis (AD), or eczema, is estimated to affect more than 30 million people in the United States, with over 6 million have moderate or severe disease. Chronic pruritus is a common symptom and is one of most difficult to manage. Even though itch is a major component in the pathology of AD, the biological underpinnings are not fully understood. In the present manuscript we identify a role for the neutrophil receptor, Mrgpra2, in the development of AD hyperplasia and chronic itch in the mouse. The role of Mrgprs in the context of itch have provided a huge step in our understanding of pruritus and have led to the development of novel therapeutics. Here we provide new evidence for the involvement of Mrgpra2 in the development of AD. Here we show that genetic deletion of Mrgpra2 significantly reduces scratching behaviors, transepidermal water loss, epidermal thickening, and Tslp expression in AD.
Follansbee, T., Le Chang, H., Larsen, Y., Kawamoto, R., Pandey, S., Dong, X.
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