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

Abstract

Fc receptor β chain (FcRβ) acts as a signaling component of FcγRIII in immune cells such as mast cells (MCs) or basophils. Recent studies reported that FcγRIII contributes to the development of arthritic inflammation. These findings suggest that FcRβ may play a pivotal role in the pathogenesis of arthritic inflammation. To address this possibility, we examined the function of FcRβ in arthritic inflammation employing a mouse model. 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 (FcRβ(+/+)) and FcRβ(-/-) mice intravenously. Three days later, 100 μg 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. Here, we demonstrate in a well-established experimental arthritis model induced by LPS and anti-CII mAbs that FcRβ(-/-) mice exhibit exacerbated arthritic inflammation manifested in paw swelling, leukocyte infiltration into the knee joint, and bone erosion and tissue cytokine expression. Our findings clearly indicate that FcRβ negatively regulates arthritic inflammation in an experimental arthritis model.