Interestingly, at active disease sites of rheumatoid arthritis and periodontitis, DCs can form aggregates with T cells in inflammatory foci, whereby they can interact through RANK-RANKL signaling in vivo, and they have been described as indirect players influencing inflammation-induced bone loss through regulating T cell activity [181–187]. The gene discussed is TNFSF11; the disease is rheumatoid arthritis.