found that in the P. gingivalis infection-induced periodontitis model, Th1 cell responses were significantly increased and promoted the secretion of the pro-inflammatory factors IFN-γ, IL-1α and IL-1β; activated Th1 cells also highly express receptor activator for nuclear factor-κB ligand (RANKL) and induce osteoclastogenesis, thus causing a widespread inflammatory response and alveolar bone destruction in periodontal tissue (Stashenko et al., 2007). The gene discussed is IL1B; the disease is periodontitis.