Activities of granulocyte-macrophage colony-stimulating factor and interleukin-3 on monocytes
Activities of granulocyte-macrophage colony-stimulating factor and interleukin-3 on monocytes
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DOI：
10.1002/ajh.20010
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发表时间：
2004-04-01
影响因子：
12.8
通讯作者：
Shiku, H
中科院分区：
文献类型：
--
作者：
Suzuki, H;Katayama, N;Shiku, H
我们使用无血清培养系统检测了粒细胞-巨噬细胞集落刺激因子（GM-CSF）和白细胞介素-3 （IL-3）对人单核细胞的作用。GM-CSF和IL-3并没有促进单核细胞向巨噬细胞的分化，而是向与未成熟树突状细胞（DCs）表型相容的细胞分化。将胎牛血清加入GM-CSF或IL-3的无血清培养物中，恢复单核细胞向巨噬细胞的分化。用GM-CSF或IL-3生成的细胞激发了吞噬活性。在GM-CSF或IL-3存在下产生的细胞，随后加入肿瘤坏死因子- α，显示成熟的dc表型，并引发和刺激免疫原性肽特异性T淋巴细胞。令人惊讶的是，GM-CSF和IL-3抑制巨噬细胞集落刺激因子（M-CSF）依赖的单核细胞向巨噬细胞的分化，并诱导分化为未成熟的dc。我们询问GM-CSF或IL-3对M-CSF依赖性向巨噬细胞分化的抑制是否与M-CSF受体（M-CSFR）的表达有关。GM-CSF或IL-3下调M-CSFR的表达。这些数据表明GM-CSF和IL-3主要支持单核细胞向DCs的分化，并通过抑制m - csf的表达抑制m - csf依赖性向巨噬细胞的分化，从而促进向DCs的分化。(C) 2004 Wiley-Liss, Inc。
We examined the actions of granulocyte-macrophage colony-stimulating factor (GM-CSF) and interleukin-3 (IL-3) on human monocytes, using a serum-free culture system. GM-CSF and IL-3 did not promote the differentiation of monocytes into macrophages but rather into cells with a phenotype compatible with that of immature dendritic cells (DCs). The addition of fetal bovine serum to serum-free cultures with GM-CSF or IL-3 restored the differentiation of monocytes into macrophages. Cells generated with GM-CSF or IL-3 elicited phagocytic activity. Cells generated in the presence of GM-CSF or IL-3, followed by the addition of tumor necrosis factor-alpha, displayed a phenotype of mature DCs, and primed and stimulated immunogenic peptide-specific T lymphocytes. Surprisingly, GM-CSF and IL-3 inhibited macrophage colony-stimulating factor (M-CSF)-dependent differentiation of monocytes into macrophages and induced differentiation into immature DCs. We asked if the inhibition of M-CSF-dependent differentiation into macrophages by GM-CSF or IL-3 was associated with the expression of M-CSF receptors (M-CSFR). GM-CSF or IL-3 down-regulated the expression of M-CSFR. These data demonstrate that GM-CSF and IL-3 primarily support the differentiation of monocytes into DCs and inhibit M-CSF-dependent differentiation into macrophages by suppressing the expression of M-CSFR, thereby promoting differentiation into DCs. (C) 2004 Wiley-Liss, Inc.