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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.
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NEOPLASIA
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
From the Department of Human Anatomy and Histology, Hematology Section, University of Bari Medical School, Bari, Italy; the Department of Internal Medicine and Public Medicine, University of Bari Medical School, Bari, Italy; and Hematology Section, University of Foggia Medical School, Foggia, Italy.
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 patients with MM, we showed that T cells support the formation of OCs with longer survival. Different from T-cell–depleted MM PBMC cultures, exogenous macrophage-colony stimulating factor (M-CSF) and receptor activator of nuclear factor- B ligand (RANKL) were necessary for the formation of OCs; however, they did not exhibit 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 (B-cell lymphoma-2/Bcl2-associated protein X) ratio, following Bcl-2 up-regulation, 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.
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