Human adipose tissue-derived mesenchymal stem cells alleviate atopic dermatitis via regulation of B lymphocyte maturation
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Tae-Hoon Shin1,2,*, Byung-Chul Lee1,2,*, Soon Won Choi1,2, Ji-Hee Shin1,2, Insung Kang1,2, Jin Young Lee1,2, Jae-Jun Kim1,2, Hong-Ki Lee3, Jae-Eon Jung3, Yong-Woon Choi3, Sung-Hoon Lee3, Jin-Sang Yoon3, Jin-Sub Choi3, Chi-Seung Lee4,5, Yoojin Seo1,4,5, Hyung-Sik Kim1,4,5, Kyung-Sun Kang1,2
1Adult Stem Cell Research Center, College of Veterinary Medicine, Seoul National University, Seoul 08826, South Korea
2Research Institute for Veterinary Science, College of Veterinary Medicine, Seoul National University, Seoul 08826, South Korea
3Biotechnology Institute, EHL-BIO Co., Ltd., Uiwang 16006, South Korea
4School of Medicine, Pusan National University, Busan 49241, South Korea
5Biomedical Research Institute, Pusan National University Hospital, Busan 49241, South Korea
*These authors contributed equally to this work
Kyung-Sun Kang, email: [email protected]
Hyung-Sik Kim, email: [email protected]
Keywords: mesenchymal stem cells, atopic dermatitis, B cell maturation, mast cell degranulation, distribution
Received: June 06, 2016 Accepted: November 12, 2016 Published: November 19, 2016
Mesenchymal stem cell (MSC) has been applied for the therapy of allergic disorders due to its beneficial immunomodulatory abilities. However, the underlying mechanisms for therapeutic efficacy are reported to be diverse according to the source of cell isolation or the route of administration. We sought to investigate the safety and the efficacy of human adipose tissue-derived MSCs (hAT-MSCs) in mouse atopic dermatitis (AD) model and to determine the distribution of cells after intravenous administration. Murine AD model was established by multiple treatment of Dermatophagoides farinae. AD mice were intravenously infused with hAT-MSCs and monitored for clinical symptoms. The administration of hAT-MSCs reduced the gross and histological signatures of AD, as well as serum IgE level. hAT-MSCs were mostly detected in lung and heart of mice within 3 days after administration and were hardly detectable at 2 weeks. All of mice administered with hAT-MSCs survived until sacrifice and did not demonstrate any adverse events. Co-culture experiments revealed that hAT-MSCs significantly inhibited the proliferation and the maturation of B lymphocytes via cyclooxygenase (COX)-2 signaling. Moreover, mast cell (MC) degranulation was suppressed by hAT-MSC. In conclusion, the intravenous infusion of hAT-MSCs can alleviate AD through the regulation of B cell function.
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