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Suppressive Effects of Mesenchymal Stem Cells in Adipose Tissue on Allergic Contact Dermatitis
( Sota Kikuchi ),( Koichi Yanaba ),( Yoshimasa Nobeyama ),( Shigeharu Yabe ),( Masahiro Kiso ),( Hidehisa Saeki ),( Yayoi Tada ),( Hidemi Nakagawa ),( Hitoshi Okochi ) 대한피부과학회 2017 Annals of Dermatology Vol.29 No.4
Background: Allergic contact dermatitis (ACD), which is ac-celerated by interferon (IFN)-γ and suppressed by inter-leukin (IL)-10 as regulators, is generally self-limited after re-moval of the contact allergen. Adipose tissue-derived multi-potent mesenchymal stem cells (ASCs) potentially exert im-munomodulatory effects. Considering that subcutaneous adipose tissue is located close to the site of ACD and includes mesenchymal stem cells (MSCs), the MSCs in adipose tissue could contribute to the self-limiting course of ACD. Objective: The aims of the present study were to elucidate the effects of MSCs in adipose tissue on ACD and to examine any cyto-kine- mediated mechanisms involved. Methods: Ear thick-ness in a C57BL/6 mouse model of ACD using contact hyper-sensitivity (CHS) elicited by 2,4,6-trinitro-1-chlorobenzene was evaluated as a marker of inflammation level. Five and nine mice were injected with ASCs and phosphate-buffered saline (PBS), respectively. After ASC or PBS injection, re-al- time reverse transcription-polymerase chain reaction and enzyme-linked immunosorbent assay were performed. Results: Histology showed that CHS was self-limited and ear thickness was suppressed by ASCs in a dose-dependent manner. IFN-γ expression in the elicited skin site and re-gional lymph nodes was significantly lower in ASC-treated mice than in control mice. IL-10 expression did not differ be-tween treated and control mice. The suppressive effects of ASCs on CHS response did not differ between IL-10 knock-out C57BL/6 mice and wild-type mice. Conclusion: The present findings suggest that MSCs in adipose tissue may contribute to the self-limiting course of ACD through de-creased expression of IFN-γ, but not through increased ex-pression of IL-10. (Ann Dermatol 29(4) 391∼399, 2017)