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The effect of pro-inflammatory cytokines on immunophenotype, differentiation capacity and immunomodulatory functions of human mesenchymal stem cells

机译：促炎细胞因子对人间充质干细胞免疫表型，分化能力和免疫调节功能的影响

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Mesenchymal stem cells (MSCs), as cells with potential clinical utilities, have demonstrated preferential incorporation into inflammation sites. Immunophenotype and immunomodulatory functions of MSCs could alter by inflamed-microenvironments due to the local pro-inflammatory cytokine milieu. A major cellular mediator with specific function in promoting inflammation and pathogenicity of autoimmunity are IL-17-producing T helper 17 (Th17) cells that polarize in inflamed sites in the presence of pro inflammatory cytokines such as Interleukin-1 beta (IL-1 beta, IL-6 and IL-23. Since MSCs are promising candidate for cell-based therapeutic strategies in inflammatory and autoimmune diseases, Th17 cell polarizing factors may alter MSCs phenotype and function. In this study, human bone-marrow-derived MSCs (BM MSC) and adipose tissue-derived MSCs (AD-MSC) were cultured with or without IL-1 beta, IL-6 and IL-23 as pro-inflammatory cytokines. The surface markers and their differentiation capacity were measured in cytokine-untreated and cytokine-treated MSCs. MSCs-mediated immunomodulation was analyzed by their regulatory effects on mixed lymphocyte reaction (MLR) and the level of IL-10, TGF-beta, IL-4, IFN-gamma and TNF-alpha production as immunomodulatory cytokines. Pro-inflammatory cytokines showed no effect on MSCs morphology, immunophenotype and co-stimulatory molecules except up-regulation of CD45. Adipogenic and osteogenic differentiation capacity increased in CD45+ MSCs. Moreover, cytokine-treated MSCs preserved the suppressive ability of allogeneic T cell proliferation and produced higher level of TGF-beta and lower level of IL-4. We concluded pro-inflammatory cytokines up-regulate the efficacy of MSCs in cell-based therapy of degenerative, inflammatory and autoimmune disorders. (C) 2016 Published by Elsevier Ltd.
机译：间充质干细胞（MSCs）作为具有潜在临床用途的细胞，已证明优先掺入炎症部位。由于局部促炎性细胞因子环境的发炎的微环境，MSC的免疫表型和免疫调节功能可能发生改变。在促进炎症和自身免疫性致病性中具有特定功能的主要细胞介质是产生IL-17的T辅助17（Th17）细胞，在促炎性细胞因子（如白介素-1 beta（IL-1 beta）存在下，在发炎部位极化，IL-6和IL-23。由于MSCs是炎症和自身免疫性疾病中基于细胞的治疗策略的有前途的候选者，因此Th17细胞极化因子可能会改变MSCs的表型和功能。在有或没有IL-1β，IL-6和IL-23作为促炎细胞因子的情况下培养MSC）和脂肪组织来源的MSC（AD-MSC），并在未处理的细胞因子中检测其表面标志物及其分化能力。通过细胞因子对混合淋巴细胞反应（MLR）的调节作用以及作为免疫调节细胞因子的IL-10，TGF-β，IL-4，IFN-γ和TNF-α的产生水平，分析了MSCs介导的免疫调节作用。促炎的除CD45上调外，细胞因子对MSC的形态，免疫表型和共刺激分子均无影响。在CD45 + MSC中，成脂和成骨分化能力增加。此外，细胞因子处理的MSC保留了同种异体T细胞增殖的抑制能力，并产生了较高水平的TGF-β和较低水平的IL-4。我们得出结论，促炎性细胞因子上调了MSC在变性，炎症和自身免疫性疾病的细胞治疗中的功效。 （C）2016由Elsevier Ltd.出版

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