Uchida Takafumi, Suto Hajime, Ra Chisei, Ogawa Hideoki, Kobata Tetsuji, Okumura Ko
Allergy Research Center, and Departments of Dermatology and Immunology, Juntendo University School of Medicine, Tokyo 113-8421, Japan.
Int Immunol. 2002 Dec;14(12):1431-8. doi: 10.1093/intimm/dxf109.
Lesional skin of patients with atopic dermatitis (AD) is histologically characterized by hypertrophy of the skin, and the infiltration of a large number of eosinophils and T cells into the dermis. Recent studies have indicated that Th2 cells play a crucial role in the pathogenesis of AD skin. Chemokines and their receptors are implicated in the development of symptoms of various skin diseases such as AD and psoriasis vulgaris (psoriasis). We have examined the in situ expression of a typical Th2-type chemokine, thymus- and activation-regulated chemokine (TARC), and its receptor (CCR4) using immunohistochemical techniques. TARC was found to be highly expressed in the basal epidermis of the lesional skin of AD patients and only slightly in the non-lesional skin. On the other hand, no positive cells were seen in the lesional skin of psoriasis. Consistently, CCR4+ cells were present predominantly in the lesional skin of AD patients, but not in the non-lesional skin. In contrast, in the lesional skin of psoriasis patients, cells positive for CCR5, which is expressed on Th1 cells, were abundantly present. Interestingly, psoralen plus ultraviolet A therapy reduced the number of CCR4+ cells in the AD skin lesions. These results suggest that Th2-type cytokines such as TARC are involved in the pathogenesis of skin lesions in AD patients through the preferential recruitment of Th2 cells.
特应性皮炎（AD）患者的皮损在组织学上表现为皮肤肥厚，大量嗜酸性粒细胞和T细胞浸润至真皮层。近期研究表明，Th2细胞在AD皮肤发病机制中起关键作用。趋化因子及其受体与多种皮肤病（如AD和寻常型银屑病）的症状发展有关。我们运用免疫组化技术检测了一种典型的Th2型趋化因子——胸腺和活化调节趋化因子（TARC）及其受体（CCR4）的原位表达。结果发现，TARC在AD患者皮损的基底表皮中高表达，而在非皮损皮肤中仅有轻微表达。另一方面，在银屑病皮损中未见阳性细胞。同样，CCR4+细胞主要存在于AD患者的皮损中，而非皮损皮肤中则没有。相反，在银屑病患者的皮损中，大量表达于Th1细胞上的CCR5阳性细胞存在。有趣的是，补骨脂素加紫外线A疗法减少了AD皮肤病变中CCR4+细胞的数量。这些结果表明，诸如TARC等Th2型细胞因子通过优先招募Th2细胞参与AD患者皮肤病变的发病机制。
