The Journal of Experimental Medicine
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Published online 11 August 2003 doi:10.1084/jem.20022220
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© Rockefeller University Press, 0022-1007/2003/8/645 $5.00
The Journal of Experimental Medicine, Volume 198, Number 4, 645-651

Brief Definitive Report

Impaired Differentiation of Osteoclasts in TREM-2–deficient Individuals

Marina Cella1, Cecilia Buonsanti1, Carey Strader1, Takayuki Kondo2, Andrea Salmaggi3 and Marco Colonna1

1 Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO
2 Department of Neurology, Fukui Redcross Hospital, 2-4-1 Tsukimi Fukui 918-8501, Japan
3 Department of Clinical Neurosciences, Istituto Nazionale Neurologico C. Besta, 20133 Milano, Italy

Address correspondence to Marco Colonna, Department of Pathology and Immunology, Washington University School of Medicine, West Building, Room 4724, Box 8118, 660 South Euclid Avenue, St. Louis, MO 63110. Phone: 314-362-0367; Fax: 314-362-4096; email: mcolonna{at}pathology.wustl.edu

TREM-2 is an immunoglobulin-like cell surface receptor associated with DAP12/KARAP that activates monocyte-derived dendritic cells (DCs) in vitro. Recently, it has been shown that genetic defects of human DAP12/KARAP and TREM-2 result in a rare syndrome characterized by bone cysts and presenile dementia called Nasu-Hakola disease. This observation suggests that TREM-2 may function in myeloid cells other than DCs, most probably osteoclasts (OCs) and microglial cells, which are involved in bone modeling and brain function. Consistent with this prediction, here we show that OC differentiation is dramatically arrested in TREM-2–deficient patients, resulting in large aggregates of immature OCs that exhibit impaired bone resorptive activity. These results demonstrate a critical role for TREM-2 in the differentiation of mononuclear myeloid precursors into functional multinucleated OCs.

Key Words: osteoclast • bone resorption • differentiation • dendritic cell • TREM


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