Only Ilr1-/- mice treated with anti-IL-36R antibody, but not Ilr1-/- or IL-36R antibody-treated wild-type mice, showed dramatically suppressed dermatitis compared to wild-type mice, indicating that both IL-1 and IL-36 are important for the induction of skin inflammation in epidermal S. aureus inoculation. The gene discussed is IL1RL2; the disease is dermatitis.