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Blood, 1 December 2004, Vol. 104, No. 12, pp. 3722-3730. Prepublished online as a Blood First Edition Paper on August 12, 2004; DOI 10.1182/blood-2004-02-0474. This Article Full Text (PDF) All Versions of this Article: 2004-02-0474v1 104/12/3722    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 Colucci, S. Articles by Grano, M. Search for Related Content PubMed PubMed Citation Articles by Colucci, S. Articles by Grano, M. Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted February 11, 2004 Accepted July 19, 2004 T cells support osteoclastogenesis in an in vitro model derived from human multiple myeloma bone disease: the role of the OPG/Trail interaction Silvia Colucci, Giacomina Brunetti, Rita Rizzi, Antonia Zonno, Giorgio Mori, Graziana Colaianni, Davide Del Prete, Roberta Faccio, Arcangelo Liso, Silvana Capalbo, Vincenzo Liso, Alberta Zallone, and Maria Grano* Department of Human Anatomy and Histology, University of Bari Medical School, Bari, Italy Hematology Section, Department of Internal Medicine and Public Medicine, University of Bari Medical School, Bari, Italy Hematology Section, University of Foggia Medical School, Foggia, Italy * Corresponding author; email: m.grano{at}anatomia.uniba.it. The development of multiple myeloma (MM) bone disease is mediated by increased number and activity of osteoclasts (OCs). Using an in vitro osteoclastogenesis model consisting of unstimulated and unfractionated peripheral blood mononuclear cells (PBMCs) from MM patients, we showed that T cells support the formation of OCs with longer survival. Differently in T cell-depleted MM PBMC cultures, exogenous macrophage-colony stimulating factor (M-CSF) and receptor activator of nuclear factor-kappa B ligand (RANKL) were necessary to the formation of OCs, not exhibiting however longer survival. We found up-regulated production of RANKL, osteoprotegerin (OPG) and TNF-related apoptosis inducing ligand (TRAIL) by fresh MM T cells. Despite high OPG levels, the persistence of osteoclastogenesis can be related to the formation of the OPG/TRAIL complex demonstrated by immunoprecipitation experiments, and the addition of anti-TRAIL antibody which decreases OC formation. OCs overexpressed TRAIL decoy receptor DcR2 in the presence of MM T cells, and death receptor DR4 in T cell-depleted cultures. In addition, increased Bcl-2/Bax ratio, following Bcl-2 upregulation, was detected in OCs generated in the presence of T cells. Our results highlight that MM T cells support OC formation and survival, possibly involving OPG/TRAIL interaction and unbalanced OC expression of TRAIL death and decoy receptors. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: P. NARDUCCI, R. BAREGGI, and V. NICOLIN Interaction of Human Recombinant Tumor Necrosis Factor-Related Apoptosis-Inducing Ligand and Osteoprotegerin Could Contribute to Enhancement of the Erosive Processes Induced by Human Synovial Cells J Rheumatol, August 1, 2009; 36(8): 1837 - 1839. [Full Text] [PDF] M. F. Faienza, G. Brunetti, S. Colucci, L. Piacente, M. Ciccarelli, L. Giordani, G. C. Del Vecchio, M. D'Amore, L. Albanese, L. Cavallo, et al. Osteoclastogenesis in Children with 21-Hydroxylase Deficiency on Long-Term Glucocorticoid Therapy: The Role of Receptor Activator of Nuclear Factor-{kappa}B Ligand/Osteoprotegerin Imbalance J. Clin. Endocrinol. Metab., July 1, 2009; 94(7): 2269 - 2276. [Abstract] [Full Text] [PDF] C. Fionda, F. Nappi, M. Piccoli, L. Frati, A. Santoni, and M. Cippitelli 15-Deoxy-{Delta}12,14-Prostaglandin J2 Negatively Regulates rankl Gene Expression in Activated T Lymphocytes: Role of NF-{kappa}B and Early Growth Response Transcription Factors J. Immunol., April 1, 2007; 178(7): 4039 - 4050. [Abstract] [Full Text] [PDF] A. R. Pettit, N. C. Walsh, C. Manning, S. R. Goldring, and E. M. Gravallese RANKL protein is expressed at the pannus-bone interface at sites of articular bone erosion in rheumatoid arthritis Rheumatology, September 1, 2006; 45(9): 1068 - 1076. [Abstract] [Full Text] [PDF] H. Ichikawa, A. Murakami, and B. B. Aggarwal 1'-Acetoxychavicol Acetate Inhibits RANKL-Induced Osteoclastic Differentiation of RAW 264.7 Monocytic Cells by Suppressing Nuclear Factor-{kappa}B Activation Mol. Cancer Res., April 1, 2006; 4(4): 275 - 281. [Abstract] [Full Text] [PDF] N. Giuliani, F. Morandi, S. Tagliaferri, S. Colla, S. Bonomini, G. Sammarelli, and V. Rizzoli Interleukin-3 (IL-3) is overexpressed by T lymphocytes in multiple myeloma patients Blood, January 15, 2006; 107(2): 841 - 842. [Full Text] [PDF] K. K. Frick, K. LaPlante, and D. A. Bushinsky RANK ligand and TNF-{alpha} mediate acid-induced bone calcium efflux in vitro Am J Physiol Renal Physiol, November 1, 2005; 289(5): F1005 - F1011. [Abstract] [Full Text] [PDF]

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