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Open Access Research article

Toll-like receptor homolog RP105 modulates the antigen-presenting cell function and regulates the development of collagen-induced arthritis

Yoshifumi Tada1*, Syuichi Koarada1, Fumitaka Morito1, Mio Mitamura1, Hisako Inoue1, Rie Suematsu1, Akihide Ohta2, Kensuke Miyake3 and Kohei Nagasawa1

Author Affiliations

1 Department of Internal Medicine, Saga Medical School, 5-1-1 Nabeshima, Saga 849-8501, Japan

2 Department of Clinical Nursing, Saga Medical School, 5-1-1 Nabeshima, Saga 849-8501, Japan

3 Division of Infectious Genetics, Institute of Medical Science, University of Tokyo, 4-6-1 Shirokanedai, Minato-ku, Tokyo 108-8639, Japan

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Arthritis Research & Therapy 2008, 10:R121  doi:10.1186/ar2529

Published: 11 October 2008

Abstract

Introduction

RP105 is a Toll-like receptor homolog expressed on B cells, dendritic cells (DCs), and macrophages. We investigated the role of RP105 in the development of collagen-induced arthritis (CIA).

Methods

CIA was induced in RP105-deficient DBA/1 mice and the incidence and arthritis index were analyzed. The cytokine production by spleen cells was determined. The functions of the DCs and regulatory T cells (Tregs) from RP105-deficient or control mice were determined by adding these cells to the lymph node cell culture. Arthritis was also induced by incomplete Freund's adjuvant (IFA) plus collagen or by injecting anti-collagen antibody and lipopolysaccharide.

Results

RP105-deficient mice showed accelerated onset of arthritis and increased severity. Interferon-gamma (IFN-γ) and tumor necrosis factor-alpha production by spleen cells from RP105-deficient mice was increased in comparison with that from wild-type mice. The DCs from RP105-deficient mice induced more IFN-γ production, whereas Tregs from those mice showed less inhibitory effect against IFN-γ production. RP105-deficient mice also showed more severe arthritis induced by collagen with IFA.

Conclusions

These results indicate that RP105 regulates the antigen-presenting cell function and Treg development, which induced the attenuation of the cell-mediated immune responses and, as a result, suppressed the development of CIA.