Benoliel A M, Capo C, Bongrand P, Ryter A, Depieds R
Immunology. 1980 Nov;41(3):547-60.
Rat peritoneal cells were made to bind test particles of five different species: immunoglobulin-coated sheep red cells (IGSRC), glutaraldehyde-treated sheep red cells (GSRC), leishmania, latex beads and tumour cells. The dependence of binding on various physicochemical parameters was studied: the binding of latex or leishmania resisted cold (4 degrees), azide, cytochalasin B, ethyleneglycol and dimethylsulphoxide (DMSO). The binding of IGSRC resisted cold and azide, but it was inhibited by cytochalasin B, ethyleneglycol and DMSO. The binding of GSRC was inhibited by cold, azide and ethyleneglycol, but not by cytochalasin B and DMSO. The binding of tumour cells was inhibited by azide, cytochalasin B, ethyleneglycol and DMSO. An attempt was made to saturate selectively some adhesive sites of macrophage membranes: glutaraldehyde-treated bovine albumin (GBSA) inhibited the ingestion of latex and GSRC, not leishmania and IGSRC, whereas a crude leishmania extract (CLE) inhibited the ingestion of all tested particles except latex. Antigen-antibody complexes inhibited the ingestion of IGSRC and leishmania, not latex and GSRC. Rat macrophages were made to bind radio-iodinated GBSA (GIBSA). The uptake of glutaraldehyde-treated albumin was proportional to the amount of substrate the cells were incubated with over a wide concentration range. This uptake was not a result of endocytosis, and it was far more efficient than that of peroxidase. Macrophage-particle interaction was studied with electron microscopy. The binding of IGSRC and leishmania to macrophages involved large areas where the interacting membranes were separated by a low density gap of constant width. The interaction of GSRC and latex with macrophages was much more patchy and irregular. Further, no redistribution of the macrophage surface polysaccharides seemed associated with the binding of GSRC. It was concluded that several different mechanisms and different membrane adhesive structures are involved in non-specific recognition by macrophages. Further, non-specific binding sometimes requires an active cell participation. Several testable hypotheses are described, which suggest further experiments in order to obtain a fuller insight into the mechanism of rosette formation.
免疫球蛋白包被的绵羊红细胞（IGSRC）、戊二醛处理的绵羊红细胞（GSRC）、利什曼原虫、乳胶珠和肿瘤细胞。研究了结合对各种物理化学参数的依赖性：乳胶或利什曼原虫的结合能抵抗低温（4℃）、叠氮化物、细胞松弛素B、乙二醇和二甲基亚砜（DMSO）。IGSRC的结合能抵抗低温和叠氮化物，但受细胞松弛素B、乙二醇和DMSO的抑制。GSRC的结合受低温、叠氮化物和乙二醇的抑制，但不受细胞松弛素B和DMSO的抑制。肿瘤细胞的结合受叠氮化物、细胞松弛素B、乙二醇和DMSO的抑制。试图选择性地饱和巨噬细胞膜的一些粘附位点：戊二醛处理的牛白蛋白（GBSA）抑制乳胶和GSRC的摄取，但不抑制利什曼原虫和IGSRC，而粗制利什曼原虫提取物（CLE）抑制除乳胶外所有测试颗粒的摄取。抗原-抗体复合物抑制IGSRC和利什曼原虫的摄取，但不抑制乳胶和GSRC。使大鼠巨噬细胞与放射性碘化的GBSA（GIBSA）结合。在很宽的浓度范围内，戊二醛处理的白蛋白的摄取量与细胞孵育的底物量成正比。这种摄取不是内吞作用的结果，并且比过氧化物酶的摄取效率高得多。用电子显微镜研究巨噬细胞-颗粒相互作用。IGSRC和利什曼原虫与巨噬细胞的结合涉及大面积区域，相互作用的膜被宽度恒定的低密度间隙隔开。GSRC和乳胶与巨噬细胞的相互作用则更为零散和不规则。此外，似乎没有观察到巨噬细胞表面多糖的重新分布与GSRC的结合有关。得出的结论是，巨噬细胞的非特异性识别涉及几种不同的机制和不同的膜粘附结构。此外，非特异性结合有时需要细胞的主动参与。描述了几个可检验的假设，这些假设建议进行进一步的实验，以便更全面地了解玫瑰花结形成的机制。
