P. gingivalis, known as a keystone pathogen in chronic periodontitis,60 employs LPS to promote immunosuppression of DCs, inducing weak DCs maturation and a Th2 bias response.39,61,62 In vitro studies have shown that P. gingivalis and its LPS can not only induce DCs to release pro-inflammatory cytokines involving IL-1β and prostaglandin E2 (PGE2), but also stimulate DCs to secrete anti-inflammatory cytokines such as IL-10 and TGF-β which induce Treg response.15E. This evidence concerns the gene TGFB1 and periodontitis.