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B 淋巴细胞作为人羊膜间充质基质细胞免疫调节特性的靶点。

B Lymphocytes as Targets of the Immunomodulatory Properties of Human Amniotic Mesenchymal Stromal Cells.

机构信息

Centro di Ricerca E. Menni, Fondazione Poliambulanza Istituto Ospedaliero, Brescia, Italy.

Department of Life Science and Public Health, Università Cattolica del Sacro Cuore, Rome, Italy.

出版信息

Front Immunol. 2020 Jun 9;11:1156. doi: 10.3389/fimmu.2020.01156. eCollection 2020.

DOI:10.3389/fimmu.2020.01156
PMID:32582218
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7295987/
Abstract

Mesenchymal stromal cells (MSC) from the amniotic membrane of human term placenta (hAMSC), and the conditioned medium generated from their culture (CM-hAMSC) offer significant tools for their use in regenerative medicine mainly due to their immunomodulatory properties. Interestingly, hAMSC and their CM have been successfully exploited in preclinical disease models of inflammatory and autoimmune diseases where depletion or modulation of B cells have been indicated as an effective treatment, such as inflammatory bowel disease, lung fibrosis, would healing, collagen-induced arthritis, and multiple sclerosis. While the interactions between hAMSC or CM-hAMSC and T lymphocytes, monocytes, dendritic cells, and macrophages has been extensively explored, how they affect B lymphocytes remains unclear. Considering that B cells are key players in the adaptive immune response and are a central component of different diseases, in this study we investigated the properties of hAMSC and CM-hAMSC on B cells. We provide evidence that both hAMSC and CM-hAMSC strongly suppressed CpG-activated B-cell proliferation. Moreover, CM-hAMSC blocked B-cell differentiation, with an increase of the proportion of mature B cells, and a reduction of antibody secreting cell formation. We observed the strong inhibition of B cell terminal differentiation into CD138 plasma cells, as further shown by a significant decrease of the expression of interferon regulatory factor 4 (), PR/SET domain 1(), and X-box binding protein 1 () genes. Our results point out that the mechanism by which CM-hAMSC impacts B cell proliferation and differentiation is mediated by secreted factors, and prostanoids are partially involved in these actions. Factors contained in the CM-hAMSC decreased the CpG-uptake sensors (CD205, CD14, and TLR9), suggesting that B cell stimulation was affected early on. CM-hAMSC also decreased the expression of interleukin-1 receptor-associated kinase (IRAK)-4, consequently inhibiting the entire CpG-induced downstream signaling pathway. Overall, these findings add insight into the mechanism of action of hAMSC and CM-hAMSC and are useful to better design their potential therapeutic application in B-cell mediated diseases.

摘要

人足月胎盘羊膜间充质干细胞(hAMSC)及其培养的条件培养基(CM-hAMSC)因其免疫调节特性而成为再生医学的重要工具。有趣的是,hAMSC 和它们的 CM 已成功地应用于炎症和自身免疫性疾病的临床前疾病模型中,在这些模型中,B 细胞的耗竭或调节已被证明是一种有效的治疗方法,如炎症性肠病、肺纤维化、伤口愈合、胶原诱导性关节炎和多发性硬化症。虽然 hAMSC 或 CM-hAMSC 与 T 淋巴细胞、单核细胞、树突状细胞和巨噬细胞之间的相互作用已经得到了广泛的研究,但它们如何影响 B 淋巴细胞仍不清楚。鉴于 B 细胞是适应性免疫反应的关键参与者,也是不同疾病的核心组成部分,在这项研究中,我们研究了 hAMSC 和 CM-hAMSC 对 B 细胞的特性。我们提供的证据表明,hAMSC 和 CM-hAMSC 均强烈抑制 CpG 激活的 B 细胞增殖。此外,CM-hAMSC 阻断 B 细胞分化,成熟 B 细胞比例增加,抗体分泌细胞形成减少。我们观察到 B 细胞向 CD138 浆细胞终末分化的强烈抑制,进一步表明干扰素调节因子 4()、PR/SET 结构域 1()和 X 盒结合蛋白 1()基因的表达显著降低。我们的研究结果表明,CM-hAMSC 影响 B 细胞增殖和分化的机制是由分泌因子介导的,前列腺素部分参与了这些作用。CM-hAMSC 中的因子降低了 CpG 摄取传感器(CD205、CD14 和 TLR9),表明 B 细胞的刺激受到了早期影响。CM-hAMSC 还降低了白细胞介素-1 受体相关激酶(IRAK)-4 的表达,从而抑制了整个 CpG 诱导的下游信号通路。总之,这些发现增加了对 hAMSC 和 CM-hAMSC 作用机制的深入了解,有助于更好地设计它们在 B 细胞介导的疾病中的潜在治疗应用。

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