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Blood, 1 May 2007, Vol. 109, No. 9, pp. 3794-3802. Prepublished online as a Blood First Edition Paper on January 3, 2007; DOI 10.1182/blood-2005-09-010116. This Article Full Text (PDF) All Versions of this Article: blood-2005-09-010116v1 109/9/3794    most recent Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Yu, J. J Articles by Gaffen, S. L Search for Related Content PubMed PubMed Citation Articles by Yu, J. J Articles by Gaffen, S. L Social Bookmarking                   What's this? Next Article  Submitted September 28, 2005 Accepted December 25, 2006 An essential role for IL-17 in preventing pathogen- initiated bone destruction: recruitment of neutrophils to inflamed bone requires IL-17 receptor-dependent signals Jeffrey J Yu, Matthew J Ruddy, Grace C Wong, Cornelia Sfintescu, Pamela J Baker, Jeffrey B Smith, Richard T Evans, and Sarah L Gaffen* Department of Microbiology and Immunology, School of Medicine and Biomedical Sciences, University at Buffalo, SUNY, Buffalo, NY, United States Department of Oral Biology, School of Dental Medicine, University at Buffalo, SUNY, Buffalo, NY, United States Department of Biology, Bates College, Lewiston, ME, United States Department of Pediatrics, David Geffen School of Medicine and Mattel Children's Hospital at UCLA, Los Angeles, CA, United States * Corresponding author; email: sgaffen{at}buffalo.edu. IL-17 and its receptor are founding members of a novel family of inflammatory cytokines. IL-17 plays a pathogenic role in rheumatoid arthritis (RA)-associated bone destruction. However, IL-17 is also an important regulator of host defense through granulopoiesis and neutrophil trafficking. Therefore, it was not obvious whether IL-17 would play a pathogenic or protective role in pathogen-initiated bone loss. The most common form of infection-induced bone destruction occurs in periodontal disease (PD). In addition to causing significant morbidity, PD is a risk factor for atherosclerotic heart disease and COPD. Similar to RA, bone destruction in PD is caused by the immune response. However, neutrophils provide critical anti-microbial defense against periodontal organisms. Since IL-17 is bone destructive in RA but a key regulator of neutrophils, we examined its role in inflammatory bone loss induced by the oral pathogen Porphyromonas gingivalis in IL-17RA-deficient mice. These mice showed enhanced periodontal bone destruction, suggesting a bone-protective role for IL-17, reminiscent of a neutrophil deficiency. Although IL-17RA-deficient neutrophils functioned normally ex vivo, IL-17RAKO mice exhibited reduced serum chemokine levels and concomitantly reduced neutrophil migration to bone. CXCR2KO mice were also highly susceptible to alveolar bone loss; interestingly, these mice also suggested a role for chemokines in maintaining normal bone homeostasis. These results indicate a non-redundant role for IL-17 in mediating host defense via neutrophil mobilization. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: Y. S. Kap, M. van Meurs, N. van Driel, G. Koopman, M.-J. Melief, H. P.M. Brok, J. D. Laman, and B. A. 't Hart A Monoclonal Antibody Selection for Immunohistochemical Examination of Lymphoid Tissues From Non-human Primates J. Histochem. 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