Human umbilical cord derived mesenchymal stem cells promote interleukin‐17 production from human peripheral blood mononuclear cells of healthy donors and systemic lupus erythematosus patients
Human umbilical cord derived mesenchymal stem cells promote interleukin‐17 production from human peripheral blood mononuclear cells of healthy donors and systemic lupus erythematosus patients
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DOI：
10.1111/cei.12737
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发表时间：
2015-10
影响因子：
4.6
通讯作者：
S. Ren;J. Hu;Y. Chen;T. Yuan;H. Hu;S. Li
中科院分区：
文献类型：
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作者：
S. Ren;J. Hu;Y. Chen;T. Yuan;H. Hu;S. Li
由白细胞介素（IL）-17-产生细胞引起的炎症是几种人类自身免疫性疾病和自身免疫动物模型的发展和发病机制的核心。据报道，来自健康供体的IL-17产生细胞的扩增由来自胎儿骨髓的间充质干细胞促进。在本研究中，检查了人脐带来源的间充质干细胞（hUC-MSCs）对健康供体和系统性红斑狼疮（SLE）患者淋巴细胞的影响。当来自健康供体的CD 4 + T细胞与hUC-MSC共培养时，产生的IL-17水平显著高于单独培养的水平。阻断实验表明，这种作用可能部分通过前列腺素E2（PGE 2）和IL-1β介导，而不涉及IL-23。然后我们将hUC-MSC与来自系统性红斑狼疮患者的人CD 4 + T细胞共培养。在SLE患者中，hUC‐ MSC在刺激的淋巴细胞中对IL-17的体外诱导显著高于健康供体。对于IL-23未观察到这种效应。综上所述，我们的结果表明，hUC-MSCs可以促进健康供体和SLE患者中CD 4 + T细胞产生IL-17。PGE 2和IL-1β也可能部分参与hUC-MSCs的促分化作用。
Inflammation instigated by interleukin (IL)‐17‐producing cells is central to the development and pathogenesis of several human autoimmune diseases and animal models of autoimmunity. The expansion of IL‐17‐producing cells from healthy donors is reportedly promoted by mesenchymal stem cells derived from fetal bone marrow. In the present study, human umbilical cord‐derived mesenchymal stem cells (hUC‐MSCs) were examined for their effects on lymphocytes from healthy donors and from patients with systemic lupus erythematosus (SLE). Significantly higher levels of IL‐17 were produced when CD4+ T cells from healthy donors were co‐cultured with hUC‐MSCs than those that were cultured alone. Blocking experiments identified that this effect might be mediated partially through prostaglandin E2 (PGE2) and IL‐1β, without IL‐23 involvement. We then co‐cultured hUC‐MSCs with human CD4+ T cells from systemic lupus erythematosus patients. Ex‐vivo inductions of IL‐17 by hUC‐MSCs in stimulated lymphocytes were significantly higher in SLE patients than in healthy donors. This effect was not observed for IL‐23. Taken together, our results represent that hUC‐MSCs can promote the IL‐17 production from CD4+ T cells in both healthy donor and SLE patients. PGE2 and IL‐1β might also be partially involved in the promotive effect of hUC‐MSCs.