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1 Department of Dermatology, Juntendo University School of Medicine, Hongo, Bunkyo-ku, Tokyo 113-8421, Japan
2 Department of Immunobiology, Meiji Pharmaceutical University, Noshio, Kiyose, Tokyo 204-8588, Japan
3 Department of Dermatology and Allergology, Juntendo University Nerima Hospital, Takanodai, Nerima-ku, Tokyo 117-0033, Japan
Correspondence
Yumi Shiraki
yshiraki{at}med.juntendo.ac.jp
Received 16 March 2006
Accepted 9 June 2006
, while T. tonsurans infection upregulated only a few genes, such as those encoding IL-1ß and IL-16. RT-PCR demonstrated that infection by both dermatophytes enhanced IL-8 mRNA expression in keratinocytes. These results suggest that A. benhamiae-induced secretion of several cytokines from keratinocytes may be involved in a severe inflammatory response, and that the limited cytokine secretion from keratinocytes in response to T. tonsurans infection may result in a minimal inflammatory response in the skin. These cytokine profiles may aid in proving the clinical features of dermatophytosis.
Abbreviations: CCR, CC chemokine receptor; GAPDH, glyceraldehyde-3-phosphate dehydrogenase; G-CSF, granulocyte-colony stimulating factor; GM-CSF, granulocyte-macrophage colony-stimulating factor; ICAM, intracellular adhesion molecule; IFN, interferon; IL, interleukin; NHEK, normal human epidermal keratinocyte; TIMP, tissue inhibitor of metalloproteinase; TNF, tumour necrosis factor.
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