Receptors for IgG complexes activate synthesis of monocyte chemoattractant peptide 1 and colony-stimulating factor 1.

Receptors for IgG complexes activate synthesis of monocyte chemoattractant peptide 1 and colony-stimulating factor 1.
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IgG 复合物的受体激活单核细胞趋化肽 1 和集落刺激因子 1 的合成。

DOI:
10.1073/pnas.89.5.1745
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发表时间:
1992
影响因子:
11.1
通讯作者:
Schlondorff,D
Schlondorff,D
中科院分区:
综合性期刊1区
文献类型:
--
作者:
Hora,K;Satriano,JA;Santiago,A;Mori,T;Stanley,ER;Shan,Z;Schlondorff,D

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在免疫复合物疾病如肾小球肾炎中负责补体非依赖性巨噬细胞积聚的趋化因子仍然未知。IgG复合物的Fc受体存在于肾脏的系膜细胞上,其产生巨噬细胞生长因子集落刺激因子1(CSF-1)。因此,我们研究了可能的刺激系膜细胞表达的CSF-1和最近确定的单核细胞特异性趋化蛋白1(MCP-1)的IgG复合物。IgG复合物,但不是单体IgG或IgG的F(ab ')2片段,在培养的小鼠系膜细胞中迅速(2-8小时)增加CSF-1(10倍)和MCP-1(20倍)的mRNA。细胞松弛素B或D均未降低CSF-1和MCP-1 mRNA的增加,表明Fc受体占据足以进行信号传导,并且不需要吞噬作用来引发这种反应。IgG复合物还导致CSF-1分泌增加10倍,MCP-1分泌增加3- 5倍。作为Fc受体占据的结果,系膜细胞合成和释放CSF-1和MCP-1可能是免疫复合物沉积部位巨噬细胞募集和活化的原因。
The chemotactic factors responsible for complement-independent macrophage accumulation in immune-complex diseases such as glomerulonephritis remain unknown. Fc receptors for IgG complexes are found on mesangial cells of the kidney, which produce the macrophage growth factor colony-stimulating factor 1 (CSF-1). We therefore investigated the possible stimulation of mesangial-cell expression of CSF-1 and the recently identified monocyte-specific chemoattractant protein 1 (MCP-1) by IgG complexes. IgG complexes, but not monomeric IgG or F(ab')2 fragments of IgG, rapidly (2-8 h) increased mRNA for both CSF-1 (10-fold) and MCP-1 (20-fold) in cultured mouse mesangial cells. The increase of mRNA for CSF-1 and MCP-1 was not reduced by either cytochalasin B or D, indicating that Fc receptor occupancy is sufficient for signaling and that phagocytosis is not required to elicit this response. IgG complexes also caused a 10-fold increase in the secretion of CSF-1 and a 3- to 5-fold increase in secretion of MCP-1 into the cell culture medium. The synthesis and release of CSF-1 and MCP-1 by mesangial cells as a consequence of Fc receptor occupancy may be responsible for macrophage recruitment and activation at sites of immune-complex deposition.