Walker F, Nicola N A, Metcalf D, Burgess A W
Cell. 1985 Nov;43(1):269-76. doi: 10.1016/0092-8674(85)90032-7.
Granulocytes and macrophages can be produced in vitro when progenitor cells from mouse bone marrow are stimulated by any of four distinct colony stimulating factors, Multi-CSF (IL-3), GM-CSF, G-CSF, and M-CSF (CSF-1). At 0 degrees C the four CSFs do not cross-compete for binding to bone marrow cells, indicating that each has a specific cell surface receptor. However, at 21 degrees C or 37 degrees C, Multi-CSF inhibits binding of the other three CSFs and GM-CSF inhibits binding of G-CSF and M-CSF. Rather than competing directly for receptor binding, the binding of Multi-CSF, GM-CSF, or G-CSF to their own receptor induces the down-modulation (and thus activation) of other CSF receptors at 37 degrees C. The pattern and potency of down-modulation activity exhibited by each type of CSF parallels the pattern and potency of its biological activity. We propose a model in which the biological interactions of the four CSFs are explained by their ability to down-modulate and activate lineage-specific receptors.
当来自小鼠骨髓的祖细胞受到四种不同的集落刺激因子（多集落刺激因子（IL-3）、粒细胞巨噬细胞集落刺激因子、粒细胞集落刺激因子和巨噬细胞集落刺激因子（CSF-1））中的任何一种刺激时，粒细胞和巨噬细胞可以在体外产生。在0℃时，这四种集落刺激因子不会相互竞争与骨髓细胞的结合，这表明每种因子都有特定的细胞表面受体。然而，在21℃或37℃时，多集落刺激因子会抑制其他三种集落刺激因子的结合，粒细胞巨噬细胞集落刺激因子会抑制粒细胞集落刺激因子和巨噬细胞集落刺激因子的结合。多集落刺激因子、粒细胞巨噬细胞集落刺激因子或粒细胞集落刺激因子与其自身受体的结合并非直接竞争受体结合，而是在37℃时诱导其他集落刺激因子受体的下调（从而激活）。每种集落刺激因子所表现出的下调活性模式和效力与其生物活性模式和效力相似。我们提出了一个模型，其中四种集落刺激因子的生物学相互作用可以通过它们下调和激活谱系特异性受体的能力来解释。
