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. Author manuscript; available in PMC: 2016 Oct 1.
Published in final edited form as: Periodontol 2000. 2015 Oct;69(1):142–159. doi: 10.1111/prd.12083

Fig. 4. The neutrostat regulatory feedback loop.

Fig. 4

IL-17 promotes granulopoiesis and mobilization of mature neutrophils from the bone marrow by acting through upregulation of granulocyte colony-stimulating factor. Upon release from the bone marrow, circulating neutrophils can normally extravasate into infected or inflamed tissues. Upon senescence, transmigrated neutrophils become apoptotic and are phagocytosed by tissue phagocytes leading to suppression of their IL-23 production, in turn, downregulating the IL-17– granulocyte colony-stimulating factor axis for maintaining steady-state neutrophil counts (140, 153). Disruption of this regulatory circuit in conditions that prevent the extravasation of neutrophils (e.g., leukocyte adhesion deficiency) leads to local overproduction of IL-17, which causes severe inflammation and periodontal bone loss (112).