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THU0027 TREM-1 stimulation inhibits human osteoclastogenesis via down-regulation of M-CSF receptor expression
  1. B. Lee1,
  2. T.-H. Kim1,
  3. E. Kwon1,
  4. S.J. Choi2,
  5. Y.H. Lee2,
  6. J. Sohn3,
  7. G.G. Song2,
  8. J.D. Ji2
  1. 1The Hanyang University Hospital for Rheumatic Diseases, Hanyang University College of Medicine
  2. 2Rheumatology
  3. 3Department of Biochemistry, College of Medicine, Korea University, Seoul, Korea, Republic Of


Background Triggering receptor expressed on myeloid cells (TREMs) are a family of cell surface receptors that play important roles in innate and adaptive immunity. Among then, TREM-2 has been extensively studied in the osteoclast differentiation and the essential role of TREM-2 in human osteoclastogenesis has been well established. However, much less has been known about the role of TREM-1 in human osteoclast differentiation.

Objectives In this study, we investigated the role of TREM-1 in human osteoclast differentiation.

Methods In vitro osteoclastogenesis assays were performed using osteoclast precursors from normal peripheral blood. Gene expressions were analyzed using real-time PCR.

Results Consistent with previous reports, TREM-2 expression was strongly increased during generation of human osteoclast precursors (pOCs). In contrast, TREM-1 expression was significantly decreased during generation of human pOCs. Stimulation of TREM-1 using agonistic TREM-1 antibody resulted in a significant suppression of RANKL-induced osteoclastogenesis, as evidenced by diminished formation of TRAP+ multinucleated cells. In addition, TREM-1 stimulation strongly suppressed RANKL-induced expression of osteoclast-related genes such as cathepsin K, integrin β3 and NFATc1. TREM-1 stimulation also down-regulated gene expression and cell surface expression of M-CSF receptor that is essential for osteoclast differentiation and survival.

Conclusions In this study, we demonstrated that TREM-1 play a negative regulator in human osteoclast differentiation and our findings identify a new mechanism of negative regulation of osteoclastogenesis that play a role during inflammation.

Disclosure of Interest None Declared

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