FcR γ 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 FcR γ subunit are essential for oxazolone-induced contact hypersensitivity, but the biological functions of the FcR γ subunit in the process of sensitisation to oxazolone remain unknown. In this study, we show that FcR γ deficiency decreases ear-swelling responses to oxazolone in mice. However, we found that oxazolone-sensitised FcR γ^−/− 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 FcR γ^−/− and WT mice showed considerable production of interferon-gamma ( IFN γ), interleukin-4 ( IL-4) and IL-17A upon oxazolone-keyhole limpet haemocyanin loading. Consistent with these data, oxazolone-sensitised FcR γ^−/− and FcR γ^+/+ LN cells conferred contact hypersensitivity to WT naïve mice challenged with the hapten. Our findings clearly indicate that, in an experimental mouse model, the FcR γ subunit positively regulates contact hypersensitivity to oxazolone without affecting the contact sensitisation process. [ABSTRACT FROM AUTHOR]