Broxmeyer H E, Bognacki J, Ralph P, Dörner M H, Lu L, Castro-Malaspina H
Blood. 1982 Sep;60(3):595-607.
The recent identification of a leukemia-associated inhibitory activity (LIA) against granulocyte-macrophage progenitor cells (CFU-GM) as acidic isoferritins has now led to detection of this activity in normal bone marrow and blood cells. Detection of this activity depends on stimulation of CFU-GM by granulocyte-macrophage colony stimulatory factors (GM-CSF), and some conditioned media (CM) sources of GM-CSF (human placental and monocyte, mouse macrophage and WEHI-3) contained low levels of acidic isoferritin that lowered colony formation. Inactivation or removal of this activity increased the stimulatory capacity of the CM. CM depleted of acidic isoferritins or CM originally devoid of this activity (human GCT, 5637, Mo, lymphocytes: mouse L cells or pokeweed-mitogen-stimulated spleen cells) increased the sensitivity of the assay to detect acidic isoferritin inhibitory activity. This activity was selectively contained and released from normal monocytes and macrophages. Restriction of this activity to mononuclear phagocytes was substantiated, as only continuous cell lines of monocytes and macrophages or lines capable of induction to this lineage contained and released acidic isoferritin inhibitory activity. The cells of origin and target cells of action suggest that acidic isoferritin-inhibitory activity can be considered as a negative feedback regulator, at least in vitro.
最近发现一种针对粒细胞-巨噬细胞祖细胞（CFU-GM）的白血病相关抑制活性（LIA）为酸性异铁蛋白，这一发现现已促使人们在正常骨髓和血细胞中检测到这种活性。这种活性的检测取决于粒细胞-巨噬细胞集落刺激因子（GM-CSF）对CFU-GM的刺激，而GM-CSF的一些条件培养基（CM）来源（人胎盘和单核细胞、小鼠巨噬细胞和WEHI-3）含有低水平的酸性异铁蛋白，会降低集落形成。这种活性的失活或去除会增加CM的刺激能力。去除酸性异铁蛋白的CM或原本缺乏这种活性的CM（人GCT、5637、Mo、淋巴细胞；小鼠L细胞或商陆丝裂原刺激的脾细胞）提高了检测酸性异铁蛋白抑制活性的检测灵敏度。这种活性选择性地存在于正常单核细胞和巨噬细胞中，并从这些细胞中释放出来。这种活性仅限于单核吞噬细胞，这一点得到了证实，因为只有单核细胞和巨噬细胞的连续细胞系或能够诱导为该谱系的细胞系含有并释放酸性异铁蛋白抑制活性。其来源细胞和作用靶细胞表明，酸性异铁蛋白抑制活性至少在体外可被视为一种负反馈调节因子。
