Imai Satoshi, Atarashi Kenji, Ikesue Koichi, Akiyama Katsuhiko, Tokura Yoshiki
Department of Dermatology, University of Occupational and Environmental Health, 1-1 Iseigaoka, Yahatanishi-ku, Kitakyushu 807-8555, Japan.
J Dermatol Sci. 2006 Feb;41(2):127-36. doi: 10.1016/j.jdermsci.2005.08.006. Epub 2005 Oct 13.
Ketoprofen is well known to evoke the allergic type of photocontact dermatitis when it is applied to the skin and irradiated with ultraviolet A (UVA) light.
We aimed to establish a murine model of this photosensitivity and to characterize pathogenic T cells concerned with the sensitivity.
Various strains of mice were sensitized on two consecutive days by application of ketoprofen to the shaved abdomen and irradiation of the skin with UVA. Five days later, they were elicited with ketoprofen plus UVA on the earlobes. Immune lymph node cells and epidermal cells from the challenged sites were analyzed by RT-PCR.
Mice were successfully sensitized and challenged with 4% and 2% ketoprofen, respective, plus UVA at 20J/cm2. The responses in H-2k mice were higher than those in the other strains examined. Immune lymph node CD4+ or CD8+ cells from ketoprofen-photosensitized H-2k mice were transferred i.v. to naïve syngeneic recipients. Mice receiving CD4+ but not CD8+ cells exhibited ketoprofen photosensitivity, but transference of both CD4+ and CD8+ cell populations was more effective. Lymph node cells from photosensitized mice expressed high levels of mRNA for Th2 cytokine (IL-4) and Th2 chemokine receptor (CCR4) as well as Th1 cytokine (IFN-gamma) and Th1 chemokine receptor (CXCR3), as assessed by RT-PCR. In addition, epidermal cells from challenged earlobes expressed increased levels of both Th1 (TARC) and Th2 (Mig) chemokines.
It is considered that not only Th1 but also Th2 cells participate in the pathogenesis of murine photocontact dermatitis to ketoprofen.
众所周知，酮洛芬应用于皮肤并接受紫外线A（UVA）照射时，会引发过敏性光接触性皮炎。
我们旨在建立这种光敏性的小鼠模型，并鉴定与该敏感性相关的致病性T细胞。
通过将酮洛芬涂抹于剃毛的腹部并进行UVA照射，连续两天使各种品系的小鼠致敏。五天后，在小鼠耳垂部位用酮洛芬加UVA进行激发。通过逆转录聚合酶链反应（RT-PCR）分析来自激发部位的免疫淋巴结细胞和表皮细胞。
分别用4%和2%的酮洛芬加20J/cm2的UVA成功使小鼠致敏并激发。H-2k小鼠的反应高于所检测的其他品系。将来自酮洛芬光敏化H-2k小鼠的免疫淋巴结CD4+或CD8+细胞静脉注射到同基因的未致敏受体小鼠体内。接受CD4+细胞而非CD8+细胞的小鼠表现出酮洛芬光敏性，但同时转移CD4+和CD8+细胞群体更有效。通过RT-PCR评估，来自光敏化小鼠的淋巴结细胞表达高水平的Th2细胞因子（IL-4）和Th2趋化因子受体（CCR4）以及Th1细胞因子（IFN-γ）和Th1趋化因子受体（CXCR3）。此外，来自激发耳垂的表皮细胞表达的Th1（TARC）和Th2（Mig）趋化因子水平均升高。
认为不仅Th1细胞而且Th2细胞都参与了小鼠对酮洛芬光接触性皮炎的发病机制。
