Interleukin‐6 Ablates the Accessory Cell‐Mediated Suppressive Effects of Lactoferrin on Human Hematopoietic Progenitor Cell Proliferation in Vitro a

Interleukin‐6 Ablates the Accessory Cell‐Mediated Suppressive Effects of Lactoferrin on Human Hematopoietic Progenitor Cell Proliferation in Vitro a
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白介素-6 消除辅助细胞介导的乳铁蛋白对体外人造血祖细胞增殖的抑制作用

DOI:
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发表时间:
1991
影响因子:
5.2
通讯作者:
H. Broxmeyer
H. Broxmeyer
中科院分区:
综合性期刊3区
文献类型:
--
作者:
P. Gentile;H. Broxmeyer

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LF是一种铁结合糖蛋白,在体内外均具有骨髓抑制作用。本研究评价了LF的体外作用方式以及各种重组CSF和IL对该作用的影响。将正常人低密度BMC(2 × 10(6)/ml)暴露于纯化的和内毒素耗尽的铁饱和LF 2小时,洗涤三次,并在rhuCSF(例如,GM-CSF、Epo、IL-3)以及在不存在和存在rhuIL-6、rhuIL-1 α或rhuIL-1 β的情况下。LF引起CFU-GM和BFU-E的40-65%的抑制平台曲线,当粘附的单核细胞(单核细胞)从靶细胞群体中去除时,该抑制平台曲线不明显。这种骨髓抑制被rhuIL-6消除,但不能被rhuIL-1 α或rhuIL-β消除。这些结果表明IL-6在辅助细胞介导的LF对CFU-GM和BFU-E的抑制作用中起作用,并开辟了IL-6可能具有造血祖细胞最佳增殖所必需的刺激/增强或辅因子活性的可能性。
LF, an iron-binding glycoprotein, has myelosuppressive effects in vitro and in vivo. The present study evaluated the mode of LF action in vitro and the effects of various recombinant CSFs and ILs on this action. Normal human low-density BMC, at 2 x 10(6)/ml, were exposed to purified and endotoxin-depleted iron-saturated LF for 2 h, washed three times, and plated for CFU-GM and BFU-E in the presence of rhuCSFs (e.g., GM-CSF, Epo, IL-3) and in the absence and presence of rhuIL-6, rhuIL-1 alpha, or rhuIL-1 beta. LF caused a 40-65% plateau curve of inhibition for CFU-GM and BFU-E that was not apparent when adherent mononuclear cells (monocytes) were removed from the target population of cells. This myelosuppression was ablated by rhuIL-6, but not by rhuIL-1 alpha or rhuIL-beta. These results suggests a role for IL-6 in the accessory cell-mediated suppressive effect of LF on CFU-GM and BFU-E and open up the possibility that IL-6 may have stimulatory/enhancing or cofactor activities necessary for optimal proliferation of hematopoietic progenitor cells.
乳铁蛋白通过抑制单核细胞释放白细胞介素 1 来减少单核细胞诱导的成纤维细胞产生骨髓集落刺激活性。
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