title: Preferential expression of T(h)2-type chemokine and its receptor in atopic dermatitis.
abstract: 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.
authors.affiliation: Allergy Research Center, and Departments of Dermatology and Immunology, Juntendo University School of Medicine, Tokyo 113-8421, Japan. kokumura@med.juntendo.ac.jp
authors.forename: Takafumi
authors.initials: T
authors.lastname: Uchida
authors.forename: Hajime
authors.initials: H
authors.lastname: Suto
authors.forename: Chisei
authors.initials: C
authors.lastname: Ra
authors.forename: Hideoki
authors.initials: H
authors.lastname: Ogawa
authors.forename: Tetsuji
authors.initials: T
authors.lastname: Kobata
authors.forename: Ko
authors.initials: K
authors.lastname: Okumura
mesh_terms: D000293:Adolescent; D000328:Adult; D054414:Chemokine CCL17; D019742:Chemokines, CC / Q000378:metabolism*; D003876:Dermatitis, Atopic / Q000378:metabolism* / Q000473:pathology; D005260:Female; D011564:Furocoumarins / Q000494:pharmacology; D005786:Gene Expression Regulation / Q000187:drug effects / Q000528:radiation effects; D006801:Humans; D008297:Male; D011701:PUVA Therapy; D054398:Receptors, CCR4; D019713:Receptors, CCR5 / Q000378:metabolism; D019707:Receptors, Chemokine; D012867:Skin / Q000378:metabolism / Q000473:pathology; D018418:Th2 Cells / Q000378:metabolism*; D014157:Transcription Factors / Q000378:metabolism*; D014466:Ultraviolet Rays
chemical_list: C106230:CCL17 protein, human; C515354:CCR4 protein, human; D054414:Chemokine CCL17; D019742:Chemokines, CC; D011564:Furocoumarins; D054398:Receptors, CCR4; D019713:Receptors, CCR5; D019707:Receptors, Chemokine; D014157:Transcription Factors