M2 differentiation of MonoMac-1 cell line induced by M-CSF and glucocorticoid pathways.

M2 differentiation of MonoMac-1 cell line induced by M-CSF and glucocorticoid pathways.
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M-CSF 和糖皮质激素途径诱导 MonoMac-1 细胞系的 M2 分化。

DOI:
10.1002/jcp.29638
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发表时间:
2020
影响因子:
5.6
通讯作者:
Rappaport,Jay
Rappaport,Jay
中科院分区:
生物学2区
文献类型:
--
作者:
Vakili,Sarah;Fischer,Tracy;Rappaport,Jay

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巨噬细胞亚型模型需要分子表征来可靠地促进它们的分化。尽管表达CD163(一种血红蛋白/触珠蛋白受体)的CD16+(Fc - γ III受体)单核细胞与多种疾病状态有关,但建立这些细胞亚型谱系所需的条件仍然未知。目前的研究利用来自急性髓性白血病谱系的细胞系MonoMac‐1来探究促进表达CD163的CD16+巨噬细胞发育的因素。结果提示糖皮质激素通路以及基于地塞米松和巨噬细胞集落刺激因子- 1作用的c - fms信号通路促进CD16+的表达,以及肉豆酸酯和脂多糖的处理。糖皮质激素和c - fms受体拮抗剂抑制CD16+细胞形成的能力进一步确定了这些途径在该细胞系中CD16表达中的作用。鉴于处理原代细胞的固有困难以及供体变异,细胞系可能比原代细胞具有一致性。我们设想,我们用于在这种细胞类型中诱导CD16表达的过程将有助于筛选和鉴定候选药物,这些候选药物可能对治疗病因涉及CD16+单核细胞亚群扩增或CD163+组织巨噬细胞积累的疾病有用。
Models of macrophage subtypes require molecular characterization to reliably facilitate their differentiation. Although CD16+(Fc‐gamma III receptor) monocytes that express CD163 (a hemoglobin/haptoglobin receptor) have been implicated in a variety of disease states, the conditions necessary to establish lineages of these cell subtypes remains unknown. The current investigations utilize a cell line derived from acute myelogenous leukemia lineage, MonoMac‐1, to interrogate the factors that promote the development of CD16+macrophages that express CD163. Results implicate the glucocorticoid pathway as well as c‐fms signaling based on the action of dexamethasone and macrophage colony‐stimulating factor‐1 in promoting CD16+expression, in addition to phorbol myristate acetate and lipopolysaccharides treatment. The ability of glucocorticoid and c‐fms receptor antagonists to inhibit CD16+cell formation further establishes the role of these pathways in CD16 expression in this cell line. In view of the inherent difficulty in working with primary cells as well as donor variation, cell lines may be preferable to primary cells for their consistency. We envision that the process we use to induce CD16 expression in this cell type will be useful for screening and identification of drug candidates potentially useful for the treatment of diseases where the etiology involves the expansion of the CD16+monocytes subset or the accumulation of CD163+tissue macrophages.
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