FcRγ promotes contact hypersensitivity to oxazolone without affecting the contact sensitisation process in B6 mice.

The process of sensitisation by specific contact allergens is indispensable for the induction of allergic contact dermatitis. Oxazolone is a well-characterised contact allergen. Previous studies suggested that immune cells bearing the FcRγ subunit are essential for oxazolone-induced contact hypersensitivity, but the biological functions of the FcRγ subunit in the process of sensitisation to oxazolone remain unknown. In this study, we show that FcRγ deficiency decreases ear-swelling responses to oxazolone in mice. However, we found that oxazolone-sensitised FcRγ(-/-) mice and oxazolone-sensitised wild-type (WT) mice have comparable numbers of CD11c(+) MHCII(hi) dendritic cells (DCs) in their draining lymph nodes (LNs). In addition, oxazolone-sensitised LN cells from both FcRγ(-/-) and WT mice showed considerable production of interferon-gamma (IFNγ), interleukin-4 (IL-4) and IL-17A upon oxazolone-keyhole limpet haemocyanin loading. Consistent with these data, oxazolone-sensitised FcRγ(-/-) and FcRγ(+/+) LN cells conferred contact hypersensitivity to WT naïve mice challenged with the hapten. Our findings clearly indicate that, in an experimental mouse model, the FcRγ subunit positively regulates contact hypersensitivity to oxazolone without affecting the contact sensitisation process.

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

OBJECTIVE: Fc receptor ß chain (FcRß) 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 FcRß may play a pivotal role in the pathogenesis of arthritic inflammation. To address this possibility, we examined the function of FcRß 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 (FcRß(+/+)) and FcRß(-/-) 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. RESULTS: Here, we demonstrate in a well-established experimental arthritis model induced by LPS and anti-CII mAbs that FcRß(-/-) 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 FcRß negatively regulates arthritic inflammation in an experimental arthritis model.