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白细胞介素-11在半固体培养中直接刺激小鼠和人类红细胞集落形成。

IL-11 directly stimulates murine and human erythroid burst formation in semisolid cultures.

作者信息

Rodriguez M H, Arnaud S, Blanchet J P

机构信息

Centre de Génétique Moléculaire et Cellulaire, CNRS UMR 106, Université Claude Bernard Lyon I, Villeurbanne, France.

出版信息

Exp Hematol. 1995 Jun;23(6):545-50.

PMID:7539382
Abstract

The effect of interleukin-11 (IL-11) on cultures of bone marrow cells was investigated. We found that IL-11 increased, in a dose-dependent manner, the number of bursts in the presence of Epo in murine or human cells cultures. This effect was also observed in cultures of murine cells established in serum-free conditions as well as in cultures of CD34+ enriched human cells in serum-containing (but not serum-free) cultures. A linear relationship between the number of bursts and the plated cell number was observed with murine bone marrow cells or non-adherent mononuclear cells (NA-MNC) human bone marrow cells. Moreover, the effect of IL-11 was not abrogated when either anti-stem cell factor-receptor (anti-SCF-R), anti-IL-3, or anti-granulocyte/macrophage colony-stimulating factor (GM-CSF), three cytokines known to greatly synergize with IL-11, was added to cultures. These results lead us to conclude that IL-11 directly stimulates the proliferation of murine and human burst-forming units-erythroid (BFU-E).

摘要

研究了白细胞介素-11(IL-11)对骨髓细胞培养的影响。我们发现,在小鼠或人类细胞培养中,IL-11在有促红细胞生成素(Epo)存在的情况下,以剂量依赖的方式增加爆式集落形成单位(BFU)的数量。在无血清条件下建立的小鼠细胞培养物以及含血清(而非无血清)培养的富集人CD34+细胞培养物中也观察到了这种效应。在小鼠骨髓细胞或非贴壁单核细胞(NA-MNC)人骨髓细胞中,观察到爆式集落形成单位数量与接种细胞数量之间存在线性关系。此外,当向培养物中添加抗干细胞因子受体(抗SCF-R)、抗IL-3或抗粒细胞/巨噬细胞集落刺激因子(GM-CSF)这三种已知与IL-11有显著协同作用的细胞因子时,IL-11的效应并未消除。这些结果使我们得出结论,IL-11直接刺激小鼠和人类红系爆式集落形成单位(BFU-E)的增殖。

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Exp Hematol. 1995 Jun;23(6):545-50.
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Transgenic Res. 2006 Feb;15(1):37-55. doi: 10.1007/s11248-005-3519-2.
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Negative cross-talk between interleukin-3 and interleukin-11 is mediated by suppressor of cytokine signalling-3 (SOCS-3).
白细胞介素-3与白细胞介素-11之间的负性相互作用由细胞因子信号转导抑制因子-3(SOCS-3)介导。
Biochem J. 2001 Jan 15;353(Pt 2):223-30. doi: 10.1042/0264-6021:3530223.