We recently reported that serum levels of interleukin (IL)-6 were increased in melanoma patients who developed neutrophil-rich psoriasiform dermatitis during immunotherapies with anti-programmed cell death 1 (PD-1) antibodies. To identify the roles of IL-6 in its pathogenesis, a murine model of imiquimod (IMQ)-induced psoriasiform dermatitis was used, by which we analyzed the difference between PD-1 deficient (PD-1-/-) mice and wild-type (WT) mice. PD-1-/- mice presented significantly more severe psoriasiform dermatitis with thicker ear swelling and higher PASI score, representing the severities of erythema, scaling and skin thickness, than WT mice (5.6 ± 0.24 v.s. 2.6 ± 0.24, P < 0.01). Histological investigations showed that more severe epidermal hyperplasia, and greater epidermal infiltration of both neutrophils and CD8 T cells in the ear samples of PD-1-/- mice than those of WT mice. PD-1-/- mice showed significantly higher mRNA levels of IL-6 and interferon (IFN)-γ in CD45-positive cells infiltrating into the epidermis, and CXCL9 in keratinocytes than WT mice. Flow cytometry analysis revealed that IL-6 productions of CD8 T cells and neutrophils were not enhanced by PD-1 deficiency. These results indicate that PD-1 deficiency enhances the infiltrating cell numbers of CD8 T cells and neutrophils, resulting in enhance of inflammation and increase of IL-6 production in the skin. The dermatitis exhibited by anti-IL-6 receptor antibody (MR16-1) treated PD-1-/- mice was significantly milder than that of isotype control IgG-treated PD-1-/- mice (PASI score; 4.3 ± 0.29 v.s. 7.3 ± 0.31 , P < 0.01), and about equal to that of isotype control IgG-treated WT mice (PASI score; 3.5 ± 0.27). In addition, MR16-1 treated PD-1-/- mice showed significantly suppressed mRNA levels in the ear skins and serum levels of psoriasis-related cytokines including IL-6, IFN-γ, IL-17A and IL-23 than those of control PD-1-/- mice. Hence, IL-6 blockade is a potential therapy to control anti-PD-1 antibody-induced psoriasisiform dermatitis.