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

被引:44
作者
Uchida, T
Suto, H
Ra, C
Ogawa, H
Kobata, T
Okumura, K [1 ]
机构
[1] Juntendo Univ, Sch Med, Dept Immunol, Tokyo 1138421, Japan
[2] Juntendo Univ, Sch Med, Allergy Res Ctr, Tokyo 1138421, Japan
[3] Juntendo Univ, Sch Med, Dept Dermatol, Tokyo 1138421, Japan
[4] Dokkyo Univ, Sch Med, Inst Med Sci, Div Immunol, Mibu, Tochigi 321293, Japan
关键词
atopic dermatitis; chemokine; chemokine receptor; T(h)1; T(h)2;
D O I
10.1093/intimm/dxf109
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
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 T(h)2 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 T(h)2-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 T(h)1 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 T(h)2-type cytokines such as TARC are involved in the pathogenesis of skin lesions in AD patients through the preferential recruitment of T(h)2 cells.
引用
收藏
页码:1431 / 1438
页数:8
相关论文
共 63 条
[11]   RELEASE OF BOTH PREFORMED AND NEWLY SYNTHESIZED TUMOR-NECROSIS-FACTOR-ALPHA (TNF-ALPHA)/CACHECTIN BY MOUSE MAST-CELLS STIMULATED VIA THE FC-EPSILON-RI - A MECHANISM FOR THE SUSTAINED ACTION OF MAST-CELL DERIVED TNF-ALPHA DURING IGE-DEPENDENT BIOLOGICAL RESPONSES [J].
GORDON, JR ;
GALLI, SJ .
JOURNAL OF EXPERIMENTAL MEDICINE, 1991, 174 (01) :103-107
[12]   Neurotic symptoms and emotional factors in atopic dermatitis [J].
Greenhill, MH ;
Finesinger, JE .
ARCHIVES OF DERMATOLOGY AND SYPHILOLOGY, 1942, 46 (02) :187-200
[13]   LESIONAL EXPRESSION OF INTERFERON-GAMMA IN ATOPIC ECZEMA [J].
GREWE, M ;
GYUFKO, K ;
SCHOPF, E ;
KRUTMANN, J .
LANCET, 1994, 343 (8888) :25-26
[14]   A role for Th1 and Th2 cells in the immunopathogenesis of atopic dermatitis [J].
Grewe, M ;
Bruijnzeel-Koomen, CAFM ;
Schöpf, E ;
Thepen, T ;
Langeveld-Wildschut, AG ;
Ruzicka, T ;
Krutmann, J .
IMMUNOLOGY TODAY, 1998, 19 (08) :359-361
[15]   TUMOR-NECROSIS-FACTOR-ALPHA IS PRO-INFLAMMATORY IN NORMAL HUMAN SKIN AND MODULATES CUTANEOUS ADHESION MOLECULE EXPRESSION [J].
GROVES, RW ;
ALLEN, MH ;
ROSS, EL ;
BARKER, JNWN ;
MACDONALD, DM .
BRITISH JOURNAL OF DERMATOLOGY, 1995, 132 (03) :345-352
[16]  
Gruber BL, 1997, J IMMUNOL, V158, P2310
[17]   Role of T cells in atopic dermatitis - New aspects on the dynamics of cytokine production and the contribution of bacterial superantigens [J].
Herz, U ;
Bunikowski, R ;
Renz, H .
INTERNATIONAL ARCHIVES OF ALLERGY AND IMMUNOLOGY, 1998, 115 (03) :179-190
[18]   The immunopharmacology of mild asthma [J].
Holgate, ST .
JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY, 1996, 98 (05) :S7-S16
[19]   The T cell-directed CC chemokine TARC is a highly specific biological ligand for CC chemokine receptor 4 [J].
Imai, T ;
Baba, M ;
Nishimura, M ;
Kakizaki, M ;
Takagi, S ;
Yoshie, O .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1997, 272 (23) :15036-15042
[20]   Selective recruitment of CCR4-bearing Th2 cells toward antigen-presenting cells by the CC chemokines thymus and activation-regulated chemokine and macrophage-derived chemokine [J].
Imai, T ;
Nagira, M ;
Takagi, S ;
Kakizaki, M ;
Nishimura, M ;
Wang, JB ;
Gray, PW ;
Matsushima, K ;
Yoshie, O .
INTERNATIONAL IMMUNOLOGY, 1999, 11 (01) :81-88