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红细胞抗体和补体包被对单核细胞介导的细胞裂解的定量影响。

Quantitative influence of antibody and complement coating of red cells on monocyte-mediated cell lysis.

作者信息

Kurlander R J, Rosse W F, Logue G L

出版信息

J Clin Invest. 1978 May;61(5):1309-19. doi: 10.1172/JCI109048.

Abstract

Monocyte-mediated lysis in vitro of human red cells coated with measured amounts of immunoglobulin G (IgG) or complement were studied. 1,000-1,500 molecules of IgG anti-D are necessary to effect measurable lysis, and lysis increases linearly with increasing levels of antibody sensitization. 100 microgram/ml of IgG1 abolished lysis even at maximal levels of anti-D sensitization (15,000 molecules/cell). Two isoimmune IgG anti-A or anti-B antisera were 5 to 10-fold less efficient in promoting phagocytosis or lysis per molecule of IgG bound; however, because of the greater antigen density of A or B, more than 100,000 molecules IgG/cell could be bound, producing equivalent lysis to anti-D-coated cells. Although inhibition by IgG1 was similar at equivalent levels of sensitization with anti-A, anti-B, or anti-D at high levels of coating with anti-A or anti-B (not attainable with anti-D), lysis was not inhibited by IgG1. Cells coated with human complement components alone were not lysed by monocytes; however, complement coating augmented IgG-mediated lysis and reduced the quantity of anti-D necessary to produce lysis to less than 1,000 molecules/cell. After thorough degradation of C3b by serum to C3d, complement augmentation persisted.

摘要

研究了单核细胞在体外对包被有定量免疫球蛋白G(IgG)或补体的人红细胞的裂解作用。要实现可测量的裂解,需要1000 - 1500个抗-D IgG分子,并且裂解程度随抗体致敏水平的增加呈线性增加。即使在抗-D致敏的最高水平(15000个分子/细胞),100μg/ml的IgG1也能消除裂解。两种同种免疫的抗-A或抗-B IgG抗血清每结合一个IgG分子促进吞噬作用或裂解的效率要低5至10倍;然而,由于A或B抗原密度更高,每细胞可结合超过100000个IgG分子,产生与抗-D包被细胞相当的裂解。尽管在高抗-A或抗-B包被水平(抗-D无法达到)下,与抗-A、抗-B或抗-D致敏的等效水平时,IgG1的抑制作用相似,但IgG1并未抑制裂解。仅包被有人补体成分的细胞不会被单核细胞裂解;然而,补体包被增强了IgG介导的裂解作用,并将产生裂解所需的抗-D量减少至小于1000个分子/细胞。在血清将C3b彻底降解为C3d后,补体增强作用仍然存在。

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本文引用的文献

7
Antibody-induced hemolytic activity of human blood monocytes.人血单核细胞的抗体诱导溶血活性。
Scand J Immunol. 1974;3(2):173-80. doi: 10.1111/j.1365-3083.1974.tb01245.x.

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