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International Immunology, Vol. 14, No. 12, pp. 1431-1438, December 2002
© 2002 Japanese Society for Immunology

Preferential expression of Th2-type chemokine and its receptor in atopic dermatitis

Takafumi Uchida1,2, Hajime Suto1,2, Chisei Ra1, Hideoki Ogawa1,2, Tetsuji Kobata4 and Ko Okumura3

1 Allergy Research Center, and Departments of 2 Dermatology and 3 Immunology, Juntendo University School of Medicine, Tokyo 113-8421, Japan 4 Division of Immunology, Institute for Medical Science, Dokkyo University School of Medicine, 880 Kitakobayashi, Mibu, Tochigi 321-293, Japan

Correspondence to: K. Okumura; E-mail: kokumura{at}med.juntendo.ac.jp
Transmitting editor: M. Miyasaka

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.

Keywords: atopic dermatitis, chemokine, chemokine receptor, Th1, Th2


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