We also showed that IL-36γ could perpetuate inflammation in human primary OECs by increasing gene expression of inflammatory cytokines (IL-1β, IL-6, TNF-α, IL-36α and IL-36γ by self-amplification) and of TLR2. This is compatible with a starting action of IL-36γ in periodontitis and could lead to an uncontrolled inflammation cascade by increasing TLR2-induced cytokines. The gene discussed is IL1B; the disease is periodontitis.