Vol.23 No.4

Original Article

Fc receptor beta chain deficiency exacerbates murine arthritis in the anti-type II collagen antibody-induced experimental model

Authors

Mino Ohtsubo-Yoshioka¹ , Satoshi Nunomura¹ , Tatsuki R. Kataoka² , Yoshimichi Okayama¹ , Chisei Ra¹

Received:

6 June 2012

Accepted:

16 August 2012

Published online:

6 October 2012

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Abstract

Objective Fc receptor b chain (FcRb) acts as a signaling component of FccRIII in immune cells such as mast cells (MCs) or basophils. Recent studies reported that FccRIII contributes to the development of arthritic inflammation. These findings suggest that FcRb may play a pivotal role in the pathogenesis of arthritic inflammation. To address this possibility, we examined the function of FcRb in arthritic inflammation employing a mouse model.
Methods For the induction of arthritis, we injected 2 mg of a cocktail of anti-type II collagen (CII) monoclonal antibodies (mAbs) into C57BL/6J mice (FcRb?/?) and FcRb-/- mice intravenously. Three days later, 100 lg lipopolysaccharide (LPS; Escherichia coli 055:B5) was intraperitoneally injected. Joint swelling was evaluated by inspection. Histopathology of joint tissues was examined by hematoxylin and eosin (H&E) or tartrate-resistant acid phosphatase staining.
Results Here, we demonstrate in a well-established experimental arthritismodel induced by LPS and anti-CIImAbs that FcRb-/- mice exhibit exacerbated arthritic inflammation manifested in paw swelling, leukocyte infiltration into the knee joint, and bone erosion and tissue cytokine expression.
Conclusion Our findings clearly indicate that FcRb negatively regulates arthritic inflammation in an experimental arthritis model.

Key words

Anti-CII mAb-induced arthritis, Fc receptor, Mast cell