Raif Geha and colleagues, at Children's Hospital, Boston, have identified a role for the protein IL-21R in a mouse model of atopic dermatitis, a common allergic inflammatory skin disease often known as eczema.
Results of their study appear online Dec. 15 in the Journal of Clinical Investigation.
As analysis of affected skin from patients with atopic dermatitis showed increased expression of IL-21R and the soluble factor that binds to it (IL-21), the authors suggest that targeting the IL-21/IL-21R interaction in the skin might help prevent skin sensitization, and therefore atopic dermatitis.
In the study, expression of IL-21R and IL-21 was increased in affected skin from patients with atopic dermatitis and in mouse skin subjected to irritation. The importance of this was highlighted by the observation that mice lacking IL-21R and normal mice treated with a molecule that blocks the IL-21/IL-21R interaction did not develop inflammation resembling atopic dermatitis after skin irritation and exposure to an allergen.
Further analysis determined one mechanism underlying the central role of IL-21R in the mouse model of atopic dermatitis. Briefly, immune cells known as DCs in the skin did not migrate to local lymph nodes and activate other immune cells important for causing the allergic inflammatory response in the skin.
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