首页> 美国政府科技报告 >Interdependence of the Radioprotective Effects of Human Recombinant Interleukin 1alpha, Tumor Necrosis Factor alpha, Granulocyte Colony-Stimulating Factor, and Murine Recombinant Granulocyte-Macrophage Colony-Stimulating Factor
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Interdependence of the Radioprotective Effects of Human Recombinant Interleukin 1alpha, Tumor Necrosis Factor alpha, Granulocyte Colony-Stimulating Factor, and Murine Recombinant Granulocyte-Macrophage Colony-Stimulating Factor

机译:人重组白细胞介素1α,肿瘤坏死因子α,粒细胞集落刺激因子和小鼠重组粒细胞 - 巨噬细胞集落刺激因子的辐射保护作用的相互依赖性

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Interleukin 1a (lL-1a), tumor necrosis factor a (TNFa), granulocyte-colony-stimulating factor (G-CSF), and granulocyte-macrophage colony-stimulating factor (GM-CSF) are molecularly distinct cytokines acting on separate receptors. The release of these cytokines can be concomitantly induced by the same signal and from the same cellular source, suggesting that they may cooperate. Administered alone, human recombinant (hr)IL-1a and hrTNFa protect lethally irradiated mice from death, whereas murine recombinant GM-CSF and hrG-CSF do not confer similar protection. On a dose basis, IL-1a is a more efficient radioprotector that TNFa. At optimal doses, IL-1a is a more radioprotective cytokine than TNFa in C57BL/6 and B6D2F1 mice and less effective than TNFa and C3H/HeN mice, suggesting that the relative effectiveness of TNFa and IL-1a depends on the genetic makeup of the host. Administration of the two cytokines in combination results in additive radioprotection in all three strains. This suggests that the two cytokines act through different radioprotective pathways and argue against their apparent redundancy. Suboptimal, nonradioprotective doses of IL-1a also synergize with GM-CSF or G-CSF to confer optimal radioprotection, suggesting that such an interaction may be necessary for radioprotection of hemopoietic progenitor cells.

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