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溶血磷脂酰胆碱处理的非贴壁细胞对巨噬细胞激活机制的作用。

Contribution of lysophosphatidylcholine-treated nonadherent cells to mechanism of macrophage activation.

作者信息

Ngwenya B Z, Yamamoto N

机构信息

Department of Microbiology and Immunology, Hahnemann University School of Medicine, Philadelphia, Pennsylvania 19102-1192.

出版信息

Proc Soc Exp Biol Med. 1990 Feb;193(2):118-24. doi: 10.3181/00379727-193-43011.

DOI:10.3181/00379727-193-43011
PMID:2300592
Abstract

Lysophosphatidylcholine (lyso-PC), a product of inflammation, stimulates (in vivo) mouse peritoneal macrophages to ingest target cells via Fc receptors. In vitro treatment of macrophages with lyso-Pc was unable to enhance ingestion activity. When a mixture of macrophages and nonadherent (B and T) cells was treated with 20 micrograms of lyso-Pc/ml for 30 min, a greatly enhanced Fc-mediated ingestion was observed at about 3 hr after treatment, suggesting that nonadherent cells contributed to activation mechanism of macrophages. The accumulated evidence suggests that treated B cells collaborated with untreated T cells in a stepwise fashion for the exchange of a signaling factor(s) for macrophage activation. When conditioned medium prepared by stepwise cultivation from treated B cells to untreated T cells was used for cultivation of untreated macrophages, a markedly enhanced Fc-mediated ingestion was observed. However, cultivation of macrophages with stepwise conditioned medium of treated T cells and untreated B cells produced no significant enhancement of phagocytic activity. Therefore, we concluded that lyso-Pc-treated B cells initiated the macrophage activation process by releasing and transmitting a signaling factor to T cells, and, in turn, the T cells modified the factor or supplied a new factor capable of the ultimate activation of macrophages for ingestion capacity. This lyso-Pc-induced factor(s) appears to be distinct from the established interleukins 1 and 2.

摘要

溶血磷脂酰胆碱(lyso-PC)是一种炎症产物,可刺激(在体内)小鼠腹腔巨噬细胞通过Fc受体摄取靶细胞。用lyso-Pc体外处理巨噬细胞无法增强摄取活性。当用20微克/毫升的lyso-Pc处理巨噬细胞和非黏附(B和T)细胞的混合物30分钟时,在处理后约3小时观察到Fc介导的摄取大大增强,这表明非黏附细胞参与了巨噬细胞的激活机制。越来越多的证据表明,经处理的B细胞与未处理的T细胞以逐步的方式协作,以交换用于巨噬细胞激活的信号因子。当使用从经处理的B细胞到未处理的T细胞逐步培养制备的条件培养基来培养未处理的巨噬细胞时,观察到Fc介导的摄取明显增强。然而,用经处理的T细胞和未处理的B细胞的逐步条件培养基培养巨噬细胞并没有显著增强吞噬活性。因此,我们得出结论,经lyso-Pc处理的B细胞通过向T细胞释放和传递信号因子启动巨噬细胞激活过程,反过来,T细胞修饰该因子或提供一种能够最终激活巨噬细胞摄取能力的新因子。这种lyso-Pc诱导的因子似乎与已确定的白细胞介素1和2不同。

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