December 31, 2008 — 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.
Source : Journal of Clinical Investigation