Opposing roles of IL-17 in inflammatory bone loss. While the dominant influence of IL-17 in RA leads to bone destruction (see Moseley et al,¹  Gaffen,²⁵  and Lubberts et al²⁸ ), we find the net effect of IL-17RA–mediated signaling in PD leads to alveolar bone protection. IL-17 is produced primarily by T cells, and triggers a variety of target cells to secrete inflammatory mediators, including chemokines, cytokines, cell-surface receptors, prostaglandin E2, and nitric oxide (NO). While many of these effectors exert bone resorptive effects by mediating enhanced osteoclastogenesis, chemokines and the neutrophils they recruit exert antimicrobial activities that ultimately lead to a bone-protective effect in the context of periodontal infection.