T-helper 2 (Th2) cells are important mediators of atopic inflammation. In addition to canonical Th2 cytokines (IL-4, -5, and -13), Th2 cells recruited to skin produce IL-31, a lesser-known cytokine associated with itch. IL-31 is detectable in skin biopsy specimens from patients with itchy inflammatory skin diseases including atopic dermatitis (AD). IL31-transgenic animals develop spontaneous scratching behaviors and eczematous skin lesions. We generated IL31-deficient animals to better define the contribution of IL-31 to Th2-driven skin inflammation. Can IL-31 regulate pro-inflammatory cytokines in addition to its direct effects on cutaneous nerves? We hypothesized that IL31-deficient mice would display reduced susceptibility to Th2-mediated inflammation in models of AD-like dermatitis. We find that exuberant CD45+ infiltrates are recruited to WT and IL31-deficient skin in response to both epithelial alarmin release and antigen-specific challenge. Surprisingly, alterations in CD4 T cell sub-populations differ by challenge type. We conclude that IL-31 plays a dynamic, non-redundant role in feedback regulation of Th2 inflammation in skin.