Cox K O, Keast D
Clin Exp Immunol. 1974 May;17(1):199-207.
The results suggest that the anaemia in mice associated with the injection of is mediated by an immune mechanism. Survival studies of Cr-labelled red blood cells (RBC) in splenectomized and unsplenectomized mice show that mice immunized with three times, clear RBC faster than unimmunized mice. However, hyperimmunized mice stabilized their haemoglobin concentrations above their minimum level and did not clear Cr-labelled RBC faster than unimmunized mice. All mice produced antibody against but remained direct Coombs'-negative. Serum from immunized animals did not contain opsonins for Cr-labelled RBC. The reticulocytosis, normal osmotic fragility tests and normal survival times of Cr-labelled RBC from -immunized mice all suggest that the main direct influence of the micro-organism is extrinsic of the RBC. Antigens from the micro-organism were adsorbed by erythrocytes . It is hypothesized that the anaemia is caused by destruction of RBC brought about by anitbody reacting with bacteria that have been adsorbed by RBC.
结果表明,与注射[具体物质未给出]相关的小鼠贫血是由免疫机制介导的。对脾切除和未脾切除小鼠体内铬标记红细胞(RBC)的存活研究表明,用[具体物质未给出]免疫三次的小鼠比未免疫小鼠更快清除红细胞。然而,过度免疫的小鼠将血红蛋白浓度稳定在其最低水平以上,并且清除铬标记红细胞的速度并不比未免疫小鼠快。所有小鼠均产生针对[具体物质未给出]的抗体,但直接抗人球蛋白试验仍为阴性。免疫动物的血清中不含有针对铬标记红细胞的调理素。来自[具体物质未给出]免疫小鼠的网织红细胞增多、正常渗透脆性试验以及铬标记红细胞的正常存活时间均表明,该微生物的主要直接影响是在红细胞外部。该微生物的抗原被红细胞[具体情况未给出]吸附。据推测,贫血是由抗体与已被红细胞吸附的细菌反应导致红细胞破坏所引起的。