Open Access

ARTICLE

Human adipose, placenta, and umbilical cord-derived mesenchymal stem cells ameliorate imiquimod-induced psoriatic mice via reducing T cells infiltration

by Jigang Lei^1,#, Zhenyao Xu^2,#, Suke Li¹, Meng Li¹, Zhikai Wang³, Ping Li¹, Jing Wang¹, Yinglu Chen¹, Xiaole Song¹, Chengjie Ren¹, Meiping Shen¹, Chengxiang Dai^1,*

1 Cellular Biomedicine Group, Shanghai, 200233, China
2 Translational Medicine Center, Shanghai General Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, 200025, China
3 Shanghai Institute of Immunology, Shanghai Jiaotong University School of Medicine, Shanghai, 200025, China

* Address correspondence to: Chengxiang Dai,
# These authors contributed equally to this work

(This article belongs to the Special Issue: Stem Cells, Protein Therapeutics, and Regenerative Medicine)

BIOCELL 2021, 45(3), 537-546. https://doi.org/10.32604/biocell.2021.014569

Received 09 October 2020; Accepted 21 December 2020; Issue published 03 March 2021

Abstract

Psoriasis is an autoimmune-related chronic inflammatory disease with an approximate prevalence of 2–3% around the world, involving increased keratinocyte proliferation. Indeed, Th17 cells and IL-17 play critical roles in the pathogenesis of psoriasis. The monoclonal antibodies against cytokines have been shown to have effectively immunosuppressive effects on human psoriasis. However, there are still some patients that have no response to these treatments. Some patients have even serious side-effects which may affect their life. Mesenchymal stem cells have the ability of immunosuppressive and anti-inflammatory effects, which may be an alternative therapy with more safety and efficacy for human psoriasis. Moreover, the underlying mechanisms by which the MSCs prevent or ameliorate psoriasis are still poorly understood. Here, we first isolated and characterized human adipose, placenta, and umbilical cord-derived mesenchymal stem cells (haMSCs, hpMSCs, and huMSCs). After that, the animal model of imiquimod (IMQ)-induced psoriasis in C57BL/6 mice was confirmed. We investigated the impact of haMSCs, hpMSCs, and huMSCs on this model by H&E staining, immunohistochemistry staining, and quantitative real-time PCR. Data analysis showed that mice subcutaneously injected with these MSCs had a significantly decreased epidermal thickness, which was caused by obviously reduced hyper-proliferation of keratinocytes. Furthermore, our findings revealed that the infiltration of T cells to psoriatic lesions in IMQ-induced psoriasis mice was markedly downregulated by intradermal administration of haMSCs, hpMSCs, and huMSCs, respectively. Consequently, the production of IL-17 from Th17 cells was reduced, which inhibits the proliferation of keratinocytes in lesioned skin of IMQ-induced psoriasis mice. These data suggest that haMSCs, hpMSCs, and huMSCs can inhibit the effects of proinflammatory Th17 cells on the development of psoriasis, which may be potential therapeutic candidates for skin inflammatory disease or other autoimmune diseases.

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