Psoriasis is a chronic, inflammatory skin disease caused by a combination of environmental and genetic factors. The Tnip1 gene encodes ABIN-1 (A20 Binding and Inhibitor of NFκB-1) protein and is strongly associated with susceptibility to psoriasis in humans. ABIN-1, a widely expressed ubiquitin binding protein, restricts TNF and TLR induced signals. We report here that mice lacking ABIN-1 specifically in dendritic cells (DCs), ABIN-1Flox CD11c-Cre mice, exhibit perturbed immune homeostasis. ABIN-1 deficient DCs display exaggerated NFκB and MAP kinase signaling and produce more IL-23 than normal cells in response to TLR ligands. Challenge of ABIN-1Flox CD11c-Cre mice with topical TLR7 ligand leads to greater numbers of TH17 and TCRγδ T cells and exacerbated development of psoriaform lesions. These phenotypes are reversed by DC-specific deletion of the TLR adaptor MyD88. These studies link ABIN-1 with IL-23 and IL-17, and provide cellular and molecular mechanisms by which ABIN-1 regulates susceptibility to psoriasis.