Nunomura Satoshi, Ohtsubo-Yoshioka Mino, Okayama Yoshimichi, Terui Tadashi, Ra Chisei
Department of Dermatology, Nihon University School of Medicine, Tokyo, Japan; Allergy and Immunology Group, Research Institute of Medical Science, Nihon University School of Medicine, Tokyo, Japan.
Exp Dermatol. 2015 Mar;24(3):204-8. doi: 10.1111/exd.12622.
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.
特定接触性变应原致敏过程对于过敏性接触性皮炎的诱发不可或缺。恶唑酮是一种特征明确的接触性变应原。既往研究提示，携带FcRγ亚基的免疫细胞对于恶唑酮诱导的接触性超敏反应至关重要，但FcRγ亚基在恶唑酮致敏过程中的生物学功能仍不清楚。在本研究中，我们发现FcRγ缺陷会降低小鼠对恶唑酮的耳部肿胀反应。然而，我们发现恶唑酮致敏的FcRγ(-/-)小鼠和恶唑酮致敏的野生型（WT）小鼠引流淋巴结（LN）中CD11c(+) MHCII(hi)树突状细胞（DC）数量相当。此外，来自FcRγ(-/-)和WT小鼠的恶唑酮致敏LN细胞在负载恶唑酮-钥孔戚血蓝蛋白后均显示出大量产生干扰素-γ（IFNγ）、白细胞介素-4（IL-4）和IL-17A。与这些数据一致，恶唑酮致敏的FcRγ(-/-)和FcRγ(+/+) LN细胞赋予接触性超敏反应给用该半抗原攻击的WT未致敏小鼠。我们的研究结果清楚地表明，在实验小鼠模型中，FcRγ亚基正向调节对恶唑酮的接触性超敏反应，而不影响接触致敏过程。
