Il31 is a cytokine involved in neuroimmune communication. It belongs to the type 2 cytokine group and is associated with multiple atopic disorders, playing a key role in pruritus, a cardinal symptom in diseases like atopic dermatitis (AD). It functions through activation of the heterodimeric receptor IL31 receptor A (IL31RA)/Oncostatin M receptor (OSMRβ), and its signaling is involved in mediating inflammatory responses, immunoregulatory circuits, and neuronal outgrowth [2].

In a mouse model of house dust mite (HDM)-induced allergic dermatitis, Il31 -deficient mice showed a deficit in HDM dermatitis-associated scratching, consistent with Il31's role as a pruritogen. However, Il31 deficiency also increased the number and proportion of cutaneous type 2 cytokine-producing CD4+ T cells and serum IgE in response to HDM. This indicates that IL-31 is an immunoregulatory factor that limits the magnitude of type 2 inflammatory responses in the skin [1].

In conclusion, Il31 is a crucial cytokine in the context of atopic and inflammatory skin diseases, especially in relation to pruritus and immunoregulation. The use of Il31-deficient mouse models has revealed its dual role in itch induction and modulation of type 2 immune responses, providing insights into the pathophysiology of allergic dermatitis and potential therapeutic targets.