Exposure to receptor-activator of NFκB ligand renders pre-osteoclasts resistant to IFN-γ by inducing terminal differentiation.docVIP

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Exposure to receptor-activator of NFκB ligand renders pre-osteoclasts resistant to IFN-γ by inducing terminal differentiation.doc

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Exposure to receptor-activator of NFκB ligand renders pre-osteoclasts resistant to IFN-γ by inducing terminal differentiation

Available online /content/5/1/R49 Open Access Exposure to receptor-activator of NFκB ligand renders pre- osteoclasts resistant to IFN- by inducing terminal differentiation Research article γ Willis Huang1, Regis J O’Keefe2 and Edward M Schwarz2 1The Department of Microbiology and Immunology, University of Rochester Medical Center, Rochester, NY, USA 2The Center for Musculoskeletal Research, University of Rochester Medical Center, Rochester, NY, USA Corresponding author: Edward M Schwarz (e-mail: edward_schwarz@) Received: 13 August 2002 Revisions received: 11 October 2002 Accepted: 14 October 2002 Published: 13 November 2002 Arthritis Res Ther 2003, 5:R49-R59 (DOI 10.1186/ar612) ? 2003 Huang et al., licensee BioMed Central Ltd (Print ISSN 1478-6354; Online ISSN 1478-6362). This is an Open Access article: verbatim copying and redistribution of this article are permitted in all media for any non-commercial purpose, provided this notice is preserved along with the articles original URL. Abstract While it has been established that IFN-γ is a strong activator of macrophages and a potent inhibitor of osteoclastogenesis in vitro, it is also known that this cytokine is produced in particular settings of inflammatory bone loss, such as infection and psoriatic arthritis. Because of the different kinetics between rapid IFN-γ macrophage activation (24 hours) and the slower production, morphological change, and surface upregulation of CD11b and receptor-activator of NFκB, suggesting that early exposure of osteoclast precursors to RANKL induces a broad resistance to the cellular effects of IFN-γ. Changes in STAT1 activation did not correlate with this resistance, as IFN-γ activated STAT1 equally in both early-stage and late-stage pre- osteoclasts. Furthermore, we failed to observe changes in TRAF6 expression following IFN-γ treatment in pre-osteoclasts. Together these data support a model of inflammatory bone loss