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Interleukin-17A upregulates receptor activator of NF-kappaB on osteoclast precursors.

Abstract：

INTRODUCTION:The interaction between the immune and skeletal systems is evidenced by the bone loss observed in autoimmune diseases such as rheumatoid arthritis. In this paper we describe a new mechanism by which the immune cytokine IL-17A directly affects osteoclastogenesis. METHODS:Human CD14+ cells were isolated from healthy donors, cultured on dentine slices and coverslips and stimulated with IL-17A and/or receptor activator of NF-kappaB ligand (RANKL). Osteoclast differentiation was evaluated by gene expression, flow cytometry, tartrate-resistant acid phosphatase staining, fluorescence and electron microscopy. Physiologic bone remodelling was studied in wild-type (Wt) and IL-17A-/- mice using micro-computer tomography and serum RANKL/osteoprotegerin concentration. Functional osteoclastogenesis assays were performed using bone marrow macrophages isolated from IL-17A-/- and Wt mice. RESULTS:IL-17A upregulates the receptor activator for NF-kappaB receptor on human osteoclast precursors in vitro, leading to increased sensitivity to RANKL signalling, osteoclast differentiation and bone loss. IL-17A-/- mice have physiological bone homeostasis indistinguishable from Wt mice, and bone marrow macrophages isolated from these mice develop fully functional normal osteoclasts. CONCLUSIONS:Collectively our data demonstrate anti-IL-17A treatment as a selective therapeutic target for bone loss associated with autoimmune diseases.

journal_name

Arthritis Res Ther

journal_title

Arthritis research & therapy

authors

Adamopoulos IE,Chao CC,Geissler R,Laface D,Blumenschein W,Iwakura Y,McClanahan T,Bowman EP

doi

10.1186/ar2936

subject

Has Abstract

pub_date

2010-01-01 00:00:00

pages

R29

issue

1

eissn

1478-6354

issn

1478-6362

pii

ar2936

journal_volume

12

pub_type

杂志文章

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