Bone marrow progenitors cultured in the presence of granulocyte-macrophage colony-stimulating factor versus macrophage colony-stimulating factor differentiate into macrophages with distinct tumoricidal capacities.
Bone marrow progenitors cultured in the presence of granulocyte-macrophage colony-stimulating factor versus macrophage colony-stimulating factor differentiate into macrophages with distinct tumoricidal capacities.
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在粒细胞-巨噬细胞集落刺激因子与巨噬细胞集落刺激因子存在下培养的骨髓祖细胞分化成具有不同杀肿瘤能力的巨噬细胞。
DOI：
10.1002/jlb.43.5.471
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发表时间：
1988
影响因子：
5.5
通讯作者：
Vogel,SN
中科院分区：
文献类型：
--
作者：
Falk,LA;Hogan,MM;Vogel,SN
在存在重组鼠粒细胞-巨噬细胞集落刺激因子（rGM-CSF）或高度纯化的鼠巨噬细胞集落刺激因子（CSF-1）的情况下培养C3 H/HeJ小鼠的骨髓源性细胞7天。在该7天培养期后，收获成熟巨噬细胞，并在不存在外源性rGM-CSF或CSF-1的情况下以精确密度重新铺板，并在双信号杀肿瘤试验中进行测定。仅用培养基或用重组干扰素-γ（rIFN-γ）作为“引发”信号和/或丁醇提取的脂多糖（But-LPS）作为“触发”信号的组合刺激培养物24小时。此时，加入51 Cr标记的P815肿瘤靶细胞，在rGM-CSF的影响下衍生的巨噬细胞表现出显著的杀肿瘤作用，与单独培养基的容量（16 ± 5%）。仅添加“启动”信号（即，rIFN-γ，10.0 U/ml）显著增加杀肿瘤能力至31 ± 9%。单独用But-LPS处理不会改变rGM-CSF衍生的巨噬细胞的基础杀肿瘤活性。rIFN-γ（10.0 U/ml）和But-LPS（0.5-5.0 μg/ml）的组合产生高度杀肿瘤的巨噬细胞（50 - 60%肿瘤细胞毒性）。相比之下，培养基处理的CSF-1衍生的巨噬细胞表现出显著较低的肿瘤细胞毒性基础水平（6 ± 3%）。与rGM-CSF衍生的巨噬细胞不同，单独用高浓度rIFN-γ处理CSF-1衍生的巨噬细胞不会显著增加细胞毒性水平，高于培养基处理的培养物。然而，CSF-I衍生的巨噬细胞对最高浓度的But-LPS（5.0 μ g/ml）作出反应，以将杀肿瘤活性从6 ± 3%增加至17 ± 5%。当用高浓度的rIFN-γ和But-LPS同时处理CSF-1衍生的巨噬细胞时，观察到最佳的杀肿瘤活性（44 ± 17%）。因此，在rGM-CSF或CSF-I中源自骨髓祖细胞的巨噬细胞表现出在基础活性以及它们对“引发”和“触发”信号的需求和敏感性方面不同的杀肿瘤能力。
Bone marrow‐derived cells from C3H/HeJ mice were cultured in the presence of recombinant murine granulocyte‐macrophage colony‐stimulating factor (rGM‐CSF) or highly purified murine macrophage colony‐stimulating factor (CSF‐1) for 7 days. Following this 7‐day culture period, mature macrophages were harvested and replated at precise densities in the absence of exogenous rGM‐CSF or CSF‐1, and assayed in a two‐signal tumoricidal assay. Cultures were stimulated with medium only or with combinations of recombinant interferon‐γ (rIFN‐γ) as the “priming” signal, and/or butanol‐extracted lipopolysaccharide (But‐LPS) as the “triggering” signal for 24 hr. At this time,51Cr‐labeled, P815 tumor target cells were added, and the percent tumor cell cytotoxicity was determined after 16 hr. Macrophages derived under the influence of rGM‐CSF exhibited significant tumoricidal capacity with medium alone (16 ± 5%). The addition of “priming” signal only (i.e., rIFN‐γ, 10.0 U/ml) significantly increased tumoricidal capacity to 31 ± 9%. Treatment with But‐LPS alone did not alter the basal tumoricidal activity of rGM‐CSF‐derived macrophages. Combinations of rIFN‐γ (10.0 U/ml) and But‐LPS (0.5–5.0 μg/ml) generated highly tumoricidal macrophages (50‐60% tumor cell cytotoxicity). In contrast, medium‐treated CSF‐1‐derived macrophages exhibited a significantly lower basal level of tumor cytotoxicity (6 ± 3%). Unlike rGM‐CSF‐derived macrophages, treatment of CSF‐1‐derived macrophages with high concentrations of rIFN‐γ alone did not increase significantly the level of cytotoxicity above that of medium‐treated cultures. However, CSF‐1‐derived macrophages responded to the highest concentrations of But‐LPS (5.0 νg/ml) to increase tumoricidal activity from 6 ± 3% to 17 ± 5%. Optimal tumoricidal activity (44 ± 17%) was observed when CSF‐1‐derived macrophages were treated simultaneously with high concentrations of both rIFN‐γ and But‐LPS. Thus, macrophages derived from bone marrow progenitors in either rGM‐CSF or CSF‐1 exhibited tumoricidal capacities that differed in basal activity as well as in their requirements for and sensitivities to “priming” and “triggering” signals.
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激活小鼠巨噬细胞杀死肿瘤细胞。
影响因子：
4.4
作者：
J. Pace;S. Russell
通讯作者：
S. Russell
影响因子：
4.4
作者：
J. Pace;S. Russell;P. A. Leblanc;D. Murasko
通讯作者：
J. Pace;S. Russell;P. A. Leblanc;D. Murasko
通过巨噬细胞激活淋巴因子诱导、维持和再诱导骨髓来源的单核吞噬细胞的杀肿瘤活性。
影响因子：
4.3
作者：
R. Keller;R. Keist
通讯作者：
R. Keist
T 细胞杂交瘤产生的巨噬细胞激活因子：理化和生物合成与γ-干扰素相似。
DOI：
--
发表时间：
1983
期刊：
Journal of immunology (Baltimore, Md. : 1950)
影响因子：
--
作者：
Schreiber,RD;Pace,JL;Russell,SW;Altman,A;Katz,DH
通讯作者：
Katz,DH
影响因子：
4.4
作者：
J. Pace;S. Russell;B. Torres;H. Johnson;P. Gray
通讯作者：
J. Pace;S. Russell;B. Torres;H. Johnson;P. Gray