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关于人淋巴细胞产物与豚鼠巨噬细胞结合的机制

On the mechanism of binding of human lymphocyte products to guinea pig macrophages.

作者信息

Weiss L, Harlos J P, Subjeck J R

出版信息

Cell Biophys. 1979 Mar;1(1):65-77. doi: 10.1007/BF02785057.

Abstract

When lymphocytes from a majority of patients with cancer are incubated with encephalitogenic factor, a lymphocyte product is released that reduces the anodic electrophoretic mobilities of guinea pig macrophages and fixed, tanned sheep erythrocytes. Although these reactions are not specific for cancer, it is distinctly possible that in patients with cancer, products from stimulated lymphocytes are capable of altering the surfaces of the patients' own macrophages, thereby modifying the course of their disease. In this paper, we attempt to elucidate some mechanisms for the binding of lymphocyte products to macrophages, such as occurs in the macrophage electrophoretic mobility (MEM) test, since this may be of general interest. Binding of lymphocyte product to macrophages has been monitored by measurements of their electrophoretic mobilities and by electron microscopic determination of the density of binding of electron-dense, cationic colloidal iron hydroxide particles to their surfaces. The results show that the lymphocyte products reduce the net surface negativity of the macrophages by (coulombic) binding of this net positively charged material to sialic acids at the macrophage surface. Product-binding can be prevented by prior treatment of the macrophages with neuraminidase. It appears that only a minority of sialic acids are involved in the binding process, which occurs without demonstrable blocking of adjacent sialic acids or redistribution of such sites over the macrophage surface. Parallel experiments with fixed tanned erythrocytes also suggest that binding of lymphocyte product is not solely determined by surface sialic acids, although it cannot occur without them.

摘要

当将大多数癌症患者的淋巴细胞与致脑炎因子一起孵育时,会释放出一种淋巴细胞产物,该产物会降低豚鼠巨噬细胞以及固定的、鞣酸处理过的绵羊红细胞的阳极电泳迁移率。尽管这些反应并非癌症所特有的,但癌症患者体内受刺激淋巴细胞产生的产物很有可能能够改变患者自身巨噬细胞的表面,从而改变其疾病进程。在本文中,我们试图阐明淋巴细胞产物与巨噬细胞结合的一些机制,比如在巨噬细胞电泳迁移率(MEM)试验中发生的情况,因为这可能具有普遍意义。通过测量巨噬细胞的电泳迁移率以及利用电子显微镜测定电子致密的阳离子氢氧化铁胶体颗粒在其表面的结合密度,来监测淋巴细胞产物与巨噬细胞的结合情况。结果表明,淋巴细胞产物通过将这种带正电的物质(库仑力)结合到巨噬细胞表面的唾液酸上,从而降低了巨噬细胞表面的净负电荷。用神经氨酸酶预先处理巨噬细胞可以阻止产物结合。似乎只有少数唾液酸参与了结合过程,该过程发生时相邻唾液酸没有明显的阻断,也没有在巨噬细胞表面重新分布这些位点。对固定的鞣酸处理过的红细胞进行的平行实验也表明,淋巴细胞产物的结合并非仅由表面唾液酸决定,尽管没有唾液酸就无法发生结合。

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