Research article

CD16 (FcRγIII) as a potential marker of osteoclast precursors in psoriatic arthritis

Yahui Grace Chiu^1,2 , Tianmeng Shao³ , Changyong Feng⁴ , Kofi A Mensah^2,5 , Michael Thullen² , Edward M Schwarz^2,5 and Christopher T Ritchlin^1,2

¹  Allergy/Immunology & Rheumatology Unit, University of Rochester Medical School, 601 Elmwood Avenue, Rochester, NY 14642, USA

²  The Center for Musculoskeletal Research, University of Rochester Medical School, 601 Elmwood Avenue, Rochester, NY 14642, USA

³  Analytical Biochemistry, MedImmune, LLC., One MedImmune Way, Gaithersburg, MD 20878, USA

⁴  Department of Biostatistics, University of Rochester Medical School, 601 Elmwood Ave., Rochester, NY 14642, USA

⁵  Department of Microbiology and Immunology, University of Rochester Medical School, 601 Elmwood Avenue, Rochester, NY 14642, USA

author email corresponding author email

Arthritis Research & Therapy 2010, 12:R14doi:10.1186/ar2915

Published:	26 January 2010

Abstract

Introduction

Psoriatic arthritis (PsA) is a chronic inflammatory arthritis characterized by bone erosion mediated by osteoclasts (OC). Our previous studies showed an elevated frequency of OC precursors (OCP) in PsA patients. Here, we examined if OC arise from CD16-positive monocytes in PsA.

Methods

Peripheral blood mononuclear cells (PBMC) or monocytes were isolated from human peripheral blood and sorted based on CD16 expression. Sorted cells were cultured alone or with bone wafers in the presence of receptor activator of nuclear factor kappa-B ligand (RANKL) and macrophage colony-stimulating factor (M-CSF). Enumeration and bone erosion activity of OC were examined after culture. The effects of tumor necrosis factor-alpha (TNFα), OC-promoting (M-CSF plus RANKL), and dendritic cell (DC)-promoting (GM-CSF plus interleukin (IL)-4) cytokines on CD16 surface expression were examined by flow cytometry.

Results

PsA and psoriasis (Ps) subjects had a higher percentage of circulating inflammatory CD14+CD16+ cells than healthy controls (HC). Exposure of cells to OC-promoting, but not DC-promoting media, was associated with CD16 up-regulation. PBMC of Ps and PsA had a higher frequency of cells expressing intermediate levels of CD16. OC were mainly derived from CD16+ cells in PsA. Increased CD16 expression was associated with a higher bone erosion activity in PsA.

Conclusions

An increased frequency of circulating CD14+CD16+ cells was noted in PsA compared to controls, and intermediate levels of CD16 may suggest a transitional state of OCP during osteoclastogenesis. Intriguingly, TNFα blocked CD16 expression on a subset of CD14+ monocytes. Collectively, our data suggest that CD16 has the potential to serve as an OCP marker in inflammatory arthritis.