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首页> 外文期刊>Clinical and Experimental Immunology: An Official Journal of the British Society for Immunology >Mesenchymal stem cells (MSCs) from scleroderma patients (SSc) preserve their immunomodulatory properties although senescent and normally induce T regulatory cells (Tregs) with a functional phenotype: Implications for cellular-based therapy
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Mesenchymal stem cells (MSCs) from scleroderma patients (SSc) preserve their immunomodulatory properties although senescent and normally induce T regulatory cells (Tregs) with a functional phenotype: Implications for cellular-based therapy

机译：硬皮病患者（SSc）的间充质干细胞（MSC）保持其免疫调节特性，尽管衰老并正常诱导具有功能表型的T调节细胞（Tregs）：对基于细胞的治疗的意义

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Systemic sclerosis (SSc) is a chronic disease, with early activation of the immune system. The aim of our work was to address how SSc-mesenchymal stem cells (MSCs), although senescent, might preserve specific immunomodulatory abilities during SSc. MSCs were obtained from 10 SSc patients and 10 healthy controls (HC). Senescence was evaluated by assessing cell cycle, β-galactosidase (β-Gal) activity, p21 and p53 expression; doxorubicin was used as acute senescence stimulus to evaluate their ability to react in stressed conditions. Immunomodulatory abilities were studied co-culturing MSCs with peripheral blood mononuclear cells (PBMCs) and CD4+ cells, in order to establish both their ability to block proliferation in mixed lymphocyte reaction and in regulatory T cells (Tregs) induction. SSc-MSC showed an increase of senescence biomarkers. Eighty per cent of MSCs were in G0-G1 phase, without significant differences between SSc and HC. SSc-MSCs showed an increased positive β-Gal staining and higher p21 transcript level compared to HC cells. After doxorubicin, β-Gal staining increased significantly in SSc-MSCs. On the contrary, doxorubicin abolished p21 activation and elicited p53 induction both in SSc- and HC-MSCs. Interleukin (IL)-6 and transforming growth factor (TGF)-β-related transcripts and their protein levels were significantly higher in SSc-MSCs. The latter maintained their immunosuppressive effect on lymphocyte proliferation and induced a functionally regulatory phenotype on T cells, increasing surface expression of CD69 and restoring the regulatory function which is impaired in SSc. Increased activation of the IL-6 pathway observed in our cells might represent an adaptive mechanism to senescence, but preserving some specific cellular functions, including immunosuppression.
机译：系统性硬化症（SSc）是一种慢性疾病，具有早期激活免疫系统的功能。我们工作的目的是解决SSc间充质干细胞（MSCs）虽衰老，但在SSc期间如何保留特定的免疫调节能力。 MSC获自10名SSc患者和10名健康对照（HC）。通过评估细胞周期，β-半乳糖苷酶（β-Gal）活性，p21和p53表达来评估衰老。阿霉素被用作急性衰老刺激，以评估其在压力条件下的反应能力。研究了将MSC与外周血单核细胞（PBMC）和CD4 +细胞共培养的免疫调节能力，以建立其在混合淋巴细胞反应和调节性T细胞（Tregs）诱导中阻断增殖的能力。 SSc-MSC显示衰老生物标志物增加。 80％的MSC处于G0-G1期，SSc和HC之间无显着差异。与HC细胞相比，SSc-MSCs表现出增强的β-Gal阳性染色和更高的p21转录水平。阿霉素治疗后，SSc-MSCs中β-Gal染色明显增加。相反，阿霉素消除了SSc-和HC-MSC中的p21激活并引起p53诱导。在SSc-MSCs中，白介素（IL）-6和转化生长因子（TGF）-β相关的转录本及其蛋白水平显着较高。后者维持其对淋巴细胞增殖的免疫抑制作用，并在T细胞上诱导功能性调节表型，增加CD69的表面表达并恢复在SSc中受损的调节功能。在我们的细胞中观察到的IL-6途径激活的增加可能代表了衰老的适应机制，但保留了某些特定的细胞功能，包括免疫抑制。

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