Possible pathogenic role of Th17 cells for atopic dermatitis.
The critical role of IL-17 has recently been reported in a variety of conditions. Since IL-17 deeply participates in the pathogenesis of psoriasis and keratinocyte production of certain cytokines, the involvement of T helper cell 17 (Th17) in atopic dermatitis (AD) is an issue to be elucidated. To evaluate the participation of Th17 cells in AD, we successfully detected circulating lymphocytes intracellularly positive for IL-17 by flow cytometry, and the IL-17+ cell population was found exclusively in CD3+CD4+ T cells. The percentage of Th17 cells was increased in peripheral blood of AD patients and associated with severity of AD. There was a significant correlation between the percentages of IL-17+ and IFN-gamma+ cells, although percentage of Th17 cells was not closely related to Th1/Th2 balance. Immunohistochemically, IL-17+ cells infiltrated in the papillary dermis of atopic eczema more markedly in the acute than chronic lesions. Finally, IL-17 stimulated keratinocytes to produce GM-CSF, TNF-alpha, IL-8, CXCL10, and VEGF. A marked synergistic effect between IL-17 and IL-22 was observed on IL-8 production. The number of Th17 cells is increased in the peripheral blood and acute lesional skin of AD. Th17 cells may exaggerate atopic eczema.
Koga
Chizuko
C
Department of Dermatology, University of Environmental and Occupational Health, Kitakyushu, Japan. Electronic address: chizu-ko@med.uoeh-u.ac.jp.
Kabashima
Kenji
K
Department of Dermatology, University of Environmental and Occupational Health, Kitakyushu, Japan. Electronic address: kkabashi@med.uoeh-u.ac.jp.
Shiraishi
Noriko
N
Department of Dermatology, University of Environmental and Occupational Health, Kitakyushu, Japan.
Kobayashi
Miwa
M
Department of Dermatology, University of Environmental and Occupational Health, Kitakyushu, Japan.
Tokura
Yoshiki
Y
Department of Dermatology, University of Environmental and Occupational Health, Kitakyushu, Japan.
D000293:Adolescent; D000328:Adult; D000368:Aged; D015496:CD4-Positive T-Lymphocytes / Q000378:metabolism / Q000473:pathology; D016022:Case-Control Studies; D002465:Cell Movement; D002648:Child; D003876:Dermatitis, Atopic / Q000209:etiology* / Q000378:metabolism* / Q000473:pathology; D020405:Dermis / Q000378:metabolism / Q000473:pathology; D005260:Female; D016178:Granulocyte-Macrophage Colony-Stimulating Factor / Q000378:metabolism; D006801:Humans; D020381:Interleukin-17 / Q000378:metabolism* / Q000494:pharmacology; D016209:Interleukin-8 / Q000378:metabolism; D007378:Interleukins / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D011565:Psoriasis / Q000378:metabolism / Q000473:pathology; D006377:T-Lymphocytes, Helper-Inducer / Q000378:metabolism* / Q000473:pathology; D018417:Th1 Cells / Q000378:metabolism / Q000473:pathology; D018418:Th2 Cells / Q000378:metabolism / Q000473:pathology; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D042461:Vascular Endothelial Growth Factor A / Q000378:metabolism; D000097043:Interleukin-22
D016178:Granulocyte-Macrophage Colony-Stimulating Factor; D020381:Interleukin-17; D016209:Interleukin-8; D007378:Interleukins; D014409:Tumor Necrosis Factor-alpha; D042461:Vascular Endothelial Growth Factor A; D000097043:Interleukin-22